| 1. |
- Malmström, P., et al.
(författare)
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Countercurrent Distribution of Lymphocytes from Human Peripheral Blood in an Aqueous Two-Phase System : I. Separation into Subsets of Lymphocytes Bearing Distinctive Markers’
- 1980
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 53, s. 39-50
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Tidskriftsartikel (refereegranskat)abstract
- Lymphocytes from human peripheral blood have been separated by countercurrent distribution in a charged aqueous two-phase system composed of Dextran T 500 and polyethylene glycol 6000 with a cell yield of 59–88% and viability above 90%. A highly reproducible partition pattern was seen with four distinct peaks. Lymphocytes with surface membrane immunoglobulin (SmIg) were located in the first part of the distribution corresponding mainly to peak I. T lymphocytes as detected by E rosetting and α-naphthyl acetate esterase (ANAE) staining showed a broad distribution with a maximum in peaks II and III. ANAE-negative lymphocytes were seen in both extremes of the distribution, corresponding to B cells in the first part and to a population of E− and SmIg− lymphocytes in the last part. Monocytes were present in all fractions with some enrichment in peaks II–IV. Lymphocytes with low-affinity Fc receptors were found in B-cell-containing fractions in the first part of the distribution, but also in the last part. Lymphocytes with high-affinity Fc receptors were detected mainly in peak IV. It is thus demonstrated that peripheral blood lymphocytes can be fractionated into subpopulations enriched in cells with characteristic markers.markers.
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| 2. |
- Malmström, P, et al.
(författare)
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Countercurrent distribution of lymphocytes from human peripheral blood in an aqueous two-phase system. : II. Separation into subsets of lymphocytes with distinctive functions
- 1980
-
Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 53, s. 51-64
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Tidskriftsartikel (refereegranskat)abstract
- Lymphocytes from human peripheral blood were separated by Countercurrent distribution (CCD) in a charged aqueous two-phase system composed of Dextran T 500 and polyethylene glycol 6000. Maximal responses to the T-cell mitogens phytohemagglutinin and concanavalin A were detected in a part of the distribution corresponding to the area where the highest percentage of E rosetting cells were seen. Antibody-dependent cellular cytotoxicity was mediated by lymphocytes located in a restricted part of the distribution separate from the majority of T lymphocytes. Lymphocytes with natural killer activity against K 562, adherent melanoma cells, and fibroblasts were detected in the same region. This area of the distribution also contained the peak of lymphocytes with high-affinity Fc receptors. It was further investigated whether affinity separation may be possible in two-phase systems on the basis of cell to cell interaction. Affinity CCD utilizing the interaction between sheep erythrocytes (SRBC) and T lymphocytes was shown to redistribute the majority of T cells into the area in which SRBC were located, while other lymphocytes were not affected. Lymphocytes mediating natural killing to adherent target cells were not redistributed, indicating that they lack high-affinity receptors for SRBC.
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| 3. |
- Miörner, Håkan, et al.
(författare)
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Regulation of mitogen-induced lymphocyte DNA synthesis by human interferon of different origins
- 1978
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 35:1, s. 15-24
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Tidskriftsartikel (refereegranskat)abstract
- Human fibroblast and leukocyte interferons were found to suppress lymphocyte mitogenesis induced by optimal doses of phytohemagglutinin and concanavalin A. In certain situations (low doses of mitogen and/or low doses of interferon), however, interferon significantly enhanced mitogenesis. In experiments using varying concentrations of interferon, dose-response curves with different slopes were obtained for fibroblast and leukocyte interferons. The effect of interferon was apparently exerted during early stages of the lymphocyte cell cycle. There was no inhibitory effect of interferon if the lymphocytes were washed with medium before being exposed to mitogen. Interferon increased the binding of radiolabeled mitogens to cells. The results suggest that the immunological effects of interferon are consequences of actions on lymphoid cells. Fibroblast and leukocyte interferons seem to have different modes of action, or to bind differently to target cells. Possible mechanisms for the suppressive and enhancing effects of interferons on lymphoid cells are discussed.
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| 4. |
- Nelson, K, et al.
(författare)
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Separation of rat leukocytes by countercurrent distribution in aqueous two-phase systems. II. Subpopulations which mediate selective and nonselective lysis of normal and colon carcinoma target cells in vitro
- 1978
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 37:2, s. 422-431
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Tidskriftsartikel (refereegranskat)abstract
- Spleen cells from WF rats immunized to allogeneic lymphoid cells or to syngeneic colon carcinomas and from unimmunized controls were separated by countercurrent distribution in aqueous two-phase systems. The cells were assayed for cytotoxicity to allogeneic fibroblasts or syngeneic colon carcinoma cells and to syngeneic fibroblasts in a 24-hr 51Cr-release assay. Cells from immunized rats which selectively lysed the specific target cells were repeatedly found in one area of the distribution separate from the majority of cells, which nonselectively lysed syngeneic fibroblasts as well. A similar subpopulation which nonselectively lysed all target cells assayed was recovered from the spleens of unimmunized rats. The cells were also assayed for the ability to lyse antibody-coated thymocytes in a 4-hr 51Cr-release assay. The peak of K cells was found to overlap partially that of cells with nonselective cytotoxicity.
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| 5. |
- Ramos, O F, et al.
(författare)
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Elevated NK-mediated lysis of Raji and Daudi cells carrying fixed iC3b fragments
- 1989
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Ingår i: Cellular Immunology. - 0008-8749 .- 1090-2163. ; 119:2, s. 459-469
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Tidskriftsartikel (refereegranskat)abstract
- Raji and Daudi cells were opsonized with C3b, iC3b and C3d fragments by using purified complement components. The sensitivity of C3-opsonized cells to lysis mediated by low density blood lymphocytes was studied. Raji and Daudi cells carrying C3b or C3d fragments were lysed with similar efficiencies as the nonopsonized cells. The presence of iC3b on the target surface imposed elevated NK sensitivity. The iC3b-mediated enhancement of NK lysis was inhibited when iC3b fragments or rabbit anti-human C3 antibodies were included into the lytic assays. These results indicate that the iC3b fragments fixed on the targets bind to the CR3 on the lymphocytes. Results obtained in immobilized conjugate-lytic assays showed that iC3b-opsonized targets interact more readily with the lymphocytes. This was reflected by the elevated proportion of lymphocytes that were bound to the iC3b-carrying targets. The proportions of conjugates in which target damage occurred were similar with the control and with the iC3b-carrying cells. It seems therefore that opsonization of targets with iC3b leads to recruitment of effector lymphocytes due to contact with their CR3. However, once the effector-target contact is established, the triggering of lytic function does not seem to be influenced by the iC3b/CR3 bridge.
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| 6. |
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| 7. |
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| 8. |
- Andersson, Eva, et al.
(författare)
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CD4+CD57+ T cells derived from peripheral blood do not support immunoglobulin production by B cells
- 1995
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 163:2, s. 245-253
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Tidskriftsartikel (refereegranskat)abstract
- A small subpopulation of CD4+ T cells found in peripheral blood coexpresses the CD57+ marker normally found on, e.g., NK cells. It is known that this population occurs in a higher frequency in certain diseases. The same antigen has also been shown to be expressed on CD4+ T cells derived from germinal centers. The localization of this cell population to specialized lymphoid structures suggests that it may play a role in the evolution of the antibody response following antigenic stimulation in vivo. We have examined the ability of peripheral blood helper T cells coexpressing CD57 to participate in B cell activation/differentiation and evaluated their responses to polyclonal stimulation. The CD4+CD57+ T cells do not express mRNA for a number of different cytokines or for the CD40 ligand after activation in vitro. Furthermore these cells do not induce differentiation of B cells into immunoglobulin-producing cells. Consequently, despite their CD4 phenotype and their ability to be activated, to express the IL-2 receptor, and to enter into the cell cycle, they do not act as T helper cells under conditions where CD4+/CD57- cells normally do so. The findings suggest that this peripheral blood helper T cell population is functionally different from regular CD4+ T cells. The basis for the lack of proper costimulatory signals for immunoglobulin production might be related to the low expression of CD28.
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| 9. |
- Andersson, Eva, et al.
(författare)
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Immunoglobulin production induced by CD57+ GC-derived helper T cells in vitro requires addition of exogenous IL-2
- 1996
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 169:2, s. 166-173
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Tidskriftsartikel (refereegranskat)abstract
- Germinal centers (GC) are well-defined areas in lymphoid organs were B cells proliferate and differentiate in response to T-cell-dependent antigens. The GC comprises B cells, follicular dendritic cells, tangible body macrophages, and a low number of CD4+ T cells. A large portion of these T cells expresses CD57. We have examined the ability of the CD4+CD57+ GC T cells to become activated and to take part in B cell activation processes, These T cells coexpress CD45RO, CD69, CD28, and upon mitogenic stimulation CD25, The cell population was found neither to containe nor to be able to produce any specific mRNA for IL-2, IL-4, and IFN-γ upon activation. Levels of mRNA encoding CD40 ligand was also undetectable under similar conditions. Furthermore, in contrast to ordinary CD4+ T cells, this population expressing CD57 was unable to induce B cells to Ig production in the presence of pokeweed mitogen or SEA unless IL-2 was added to the cultures, However, despite their apparent lack of function CD4+CD57+ GC T cells were found to rescue GC B cells from cell death in vitro to the same extent as CD4+CD57- T(h) cells, The phenotypical and functional differences found between these T cells and regular T(h)-cells suggest that they either represent a T cell subset with distinct properties within the GC yet to be determined or that they represent T cells, Irate in the immune response, having lost most of their original functions and capabilities.
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| 10. |
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| 11. |
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| 12. |
- Barathan, Muttiah, et al.
(författare)
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CD8+T cells of chronic HCV-infected patients express multiple negative immune checkpoints following stimulation with HCV peptides
- 2017
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Ingår i: Cellular Immunology. - : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 0008-8749 .- 1090-2163. ; 313
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Tidskriftsartikel (refereegranskat)abstract
- Hepatitis C virus (HCV)-specific CD4+ and CD8+ T cells are key to successful viral clearance in HCV disease. Accumulation of exhausted HCV-specific T cells during chronic infection results in considerable loss of protective functional immune responses. The role of T-cell exhaustion in chronic HCV disease remains poorly understood. Here, we studied the frequency of HCV peptide-stimulated T cells expressing negative immune checkpoints (PD-1, CTLA-4, TRAIL, TIM-3 and BTLA) by flow cytometry, and measured the levels of Th1/Th2/Th17 cytokines secreted by T cells by a commercial Multi-Analyte ELISArray (TM) following in vitro stimulation of T cells using HCV peptides and phytohemagglutinin (PHA). HCV peptide stimulated CD4+ and CD8+ T cells of chronic HCV (CHC) patients showed significant increase of CTLA-4. Furthermore, HCV peptide-stimulated CD4+ T cells of CHC patients also displayed relatively higher levels of PD-1 and TRAIL, whereas TIM-3 was up-regulated on HCV peptide-stimulated CD8+ T cells. Whereas the levels of IL-10 and TGF-beta 1 were significantly increased, the levels of pro-inflammatory cytokines IL-2, TNF-alpha, IL-17A and IL-6 were markedly decreased in the T cell cultures of CHC patients. Chronic HCV infection results in functional exhaustion of CD4+ and CD8+ T cells likely contributing to viral persistence. (C) 2016 Elsevier Inc. All rights reserved.
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| 13. |
- Berglund, Martin, 1979, et al.
(författare)
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Gender dependent importance of IRAK-1 in dextran sulfate sodium induced colitis
- 2009
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Ingår i: Cellular Immunology. - : Elsevier BV. - 1090-2163 .- 0008-8749. ; 259:1, s. 27-32
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Tidskriftsartikel (refereegranskat)abstract
- Toll-like receptor (TLR) signaling is important for the induction of pro-inflammatory cytokines and interferon (IFN)-inducible genes in response to bacterial and viral challenge. Interleukin-1 receptor-associated kinase-1 (IRAK-1) is a signaling kinase situated downstream of the adapter protein myeloid differentiation factor 88 (MyD88) in the TLR intracellular signaling cascade and is required for normal signal transduction through this pathway. We investigated the importance of IRAK-1 in intestinal inflammation by using the dextran sulfate sodium (DSS)-colitis model. We show that IRAK-1 deficient mice are protected against systemic signs of inflammation, i.e., weight loss and spleen enlargement compared to wild-type controls irrespective of gender. However, IRAK-1(-/y) males but not IRAK-1(-/-) females display significant protection against colitis and thymic atrophy compared to wild-type mice. Our results indicate a gender specific effect of IRAK-1 in the DSS-induced colitis, an interesting finding since the Irak-1 gene is located on the X-chromosome and several inflammatory diseases have a gender dependent incidence.
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| 14. |
- Bjursten, Malin, 1976, et al.
(författare)
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Enhanced pro-inflammatory cytokine production in Galphai2-deficient mice on colitis prone and colitis resistant 129Sv genetic backgrounds.
- 2004
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Ingår i: Cellular immunology. - : Elsevier BV. - 0008-8749. ; 228:2, s. 77-80
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Tidskriftsartikel (refereegranskat)abstract
- Mice deficient in G-protein subunit alphai2 develop colitis closely resembling human ulcerative colitis when raised on 129SvEv background. When backcrossing the Galphai2-deficiency into a 129SvJBom genetic background, surprisingly, mice did not develop colitis. In vitro stimulation of splenocytes with formalin-killed Staphylococcus aureus resulted in significantly increased production of interleukin-1beta, tumor necrosis factor, and interleukin-12p40 in Galphai2(-/-) as compared to control mice. The enhanced production of pro-inflammatory cytokines was seen in colitis prone as well as in colitis resistant genetic background. A similar outcome was seen upon stimulation with toxic shock syndrome toxin-1, a T cell superantigen, except that Galphai2(-/-) colitis resistant 129SvJBom splenocytes did not show increased production of IL-12p40 as compared to their controls.
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| 15. |
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| 16. |
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| 17. |
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| 18. |
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| 19. |
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| 20. |
- Hellman, Per, et al.
(författare)
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Ligand surface density is important for efficient capture of immunoglobulin and phosphatidylcholine coated particles by human peripheral dendritic cells
- 2009
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749 .- 1090-2163. ; 258:2, s. 123-30
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Tidskriftsartikel (refereegranskat)abstract
- A unique property of dealuminated zeolite particles is the exceptional ability to bind both hydrophilic and hydrophobic biomolecules without any covalent linkages. By adsorbing phospholipids onto the particle surface, capture of particles by human peripheral myeloid dendritic cells (mDCs) was observed. Capture of zeolite particles was only seen when a low density of phosphatidylcholine was present on the particles, indicating a specific recognition of the structural features realised by phosphatidylcholine after adsorption on the particle. Adsorbing IgG on the particles revealed capture by mDCs that was dependent upon the density of the IgG molecules. To obtain a smaller particle exposing a high density of IgG molecules, immune complexes (ICs) were formed and both mDCs and pDCs (peripheral plasmacytoid DCs) captured immune complexes, although the mDCs showed a more efficient capture of ICs. As expected, mDCs captured and internalized ICs, whereas pDCs captured ICs but showed no internalization of ICs.
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| 21. |
- Hultqvist, Malin, et al.
(författare)
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Ncf1 (p47phox) polymorphism determines oxidative burst and the severity of arthritis in rats and mice.
- 2005
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 233:2, s. 97-101
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Tidskriftsartikel (refereegranskat)abstract
- Identifying genes that regulate polygenic diseases influenced by the environment such as rheumatoid arthritis (RA), has so far proven to be difficult. By using an alternative approach, i.e., linkage analysis using relevant animal models we succeeded in finding the Ncf1 gene residing in the Pia4 quantitative trait locus to be responsible for the severity of pristane induced arthritis in rats. The influence of another mutation in the mouse Ncf1 gene showed the same association between decreased oxidative burst and enhanced arthritis. In this case the mutation affected a splice site giving a non-detectable oxidative burst response and enhanced collagen induced arthritis as well as myelin oligodendrocyte protein induced experimental autoimmune encephalomyelitis. These findings open up new possibilities for new treatments for autoimmune diseases, i.e., RA, targeting the NADPH oxidase pathway.
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| 22. |
- Johansson, A, et al.
(författare)
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Different subcellular localization of cytochrome b and the dormant NADPH-oxidase in neutrophils and macrophages: effect on the production of reactive oxygen species during phagocytosis.
- 1995
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Ingår i: Cellular immunology. - : Elsevier BV. - 0008-8749. ; 161:1, s. 61-71
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Tidskriftsartikel (refereegranskat)abstract
- When neutrophils and macrophages phagocytose a prey, e.g., complement (C3b)-opsonized yeast particles, the oxygen radical generating NADPH-oxidase is activated. In neutrophils, most of the production of oxygen metabolites occurred in an intracellular compartment, possibly in the phagolysosome. In contrast, no intracellular production could be detected in human macrophages. In these cells, the subcellular localization of the superoxide-generating NADPH-oxidase and associated cytochrome b was assessed in intact cells with indirect immunofluorescence and confocal laser scanning microscopy, and with subcellular fractionation, using centrifugation on Percoll density gradients. A dual localization of the cytochrome b as well as the dormant NADPH-oxidase activity in neutrophils was in agreement with earlier immunocytochemical, biochemical, and subcellular fractionation studies. Furthermore, most of the activity was recovered from the specific granules, whereas only a small fraction was retained in the plasma membrane. In contrast, the cytochrome b/NADPH-oxidase activity in macrophages localized primarily in the plasma membrane fraction. We suggest that the macrophages are incapable of producing reactive oxygen species intraphagosomally, due to an absence of a granule-localized pool of the membrane components of the NADPH-oxidase.
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| 23. |
- Johansson, Susanne E, et al.
(författare)
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Accumulation and activation of natural killer cells in local intraperitoneal HIV-1/MuLV infection results in early control of virus infected cells
- 2011
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749 .- 1090-2163. ; 272:1, s. 71-78
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Tidskriftsartikel (refereegranskat)abstract
- Natural killer (NK) cells are important effectors in resistance to viral infections. The role of NK cells in the acute response to human immunodeficiency virus 1 (HIV-1) infected cells was investigated in a mouse model based on a HIV-1/murine leukemia virus (MuLV) pseudovirus. Splenocytes infected with HIV-1/MuLV were injected intraperitoneally and local immunologic responses and persistence of infected cells were investigated. In vivo depletion with an anti-NK1.1 antibody showed that NK cells are important in resistance to virus infected cells. Moreover, NK cell frequency in the peritoneal cavity increased in response to infected cells and these NK cells had a more mature phenotype, as determined by CD27 and Mac-1 expression. Interestingly, after injection of HIV-1/MuLV infected cells, but not MuLV infected cells, peritoneal NK cells had an increased cytotoxic activity.
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| 24. |
- Jonsson, Charlotte A, 1971, et al.
(författare)
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Mycophenolate mofetil ameliorates perivascular T lymphocyte inflammation and reduces the double-negative T cell population in SLE-prone MRLlpr/lpr mice.
- 1999
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Ingår i: Cellular immunology. - : Elsevier BV. - 0008-8749. ; 197:2, s. 136-44
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Tidskriftsartikel (refereegranskat)abstract
- Effects on T lymphocyte mediated pathology, phenotypes, and functions in MRLlpr/lpr mice given mycophenolate mofetil (MMF) (100 mg/kg/day) via drinking water or controls given ip cyclophosphamide (CYC) injections (1.8 mg/mouse/week) or water were described. Both MMF and CYC treatment diminished kidney and large salivary gland perivascular cell infiltrates, reduced profoundly double-negative (DN) T cell frequencies, decreased total lymphocyte number in spleen, and increased in vitro proliferative response to Con A. IFN-gamma and IL-10 in supernatants from Con A stimulated spleen cells were augmented after MMF but not CYC treatment. MMF treatment increased whereas CYC reduced IL-12 in serum. Kidney expressions of IFN-gamma, IL-10, and IL-12 mRNA were unaffected by MMF but decreased by CYC. Our results demonstrate that MMF and CYC suppress perivascular T lymphocyte inflammation by reducing the DN T cell population and by amelioration of T cell function. The varying cytokine patterns suggest different mechanisms of the two drugs.
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| 25. |
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| 26. |
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| 27. |
- Kerzeli, Iliana K., et al.
(författare)
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MALT1 inhibition suppresses antigen-specific T cell responses
- 2024
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Ingår i: Cellular Immunology. - : Elsevier. - 0008-8749 .- 1090-2163. ; 397
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to assess the potential use of a selective small molecule MALT1 inhibitor in solid tumor treatment as an immunotherapy targeting regulatory T-cells (Tregs). In vitro, MALT1 inhibition suppressed the proteolytic cleavage of the MALT1-substrate HOIL1 and blocked IL-2 secretion in Jurkat cells. It selectively suppressed the proliferation of PBMC-derived Tregs, with no effect on conventional CD4+ T-cells. In vivo, however, no evident anti-tumor effect was achieved by MALT1 inhibition monotherapy or in combination with anti-CTLA4 in the MB49 cancer model. Despite decreased Treg-frequencies in lymph nodes of tumor-bearing animals, intratumoral Treg depletion was not observed. We also showed that MALT1-inhibition caused a reduction of antigen-specific CD8+ T-cells in an adoptive T-cell transfer model. Thus, selective targeting of Tregs would be required to improve the immunotherapeutic effect of MALT1-inhibition. Also, various dosing schedules and combination therapy strategies should be carefully designed and evaluated further.
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| 28. |
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| 29. |
- Lindberg, Erika, 1979, et al.
(författare)
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Impaired activation of IFN-gamma+CD4+ T cells in peripheral blood of patients with dilated cardiomyopathy
- 2010
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Ingår i: Cellular Immunology. - San Diego, USA : Elsevier. - 0008-8749 .- 1090-2163. ; 263:2, s. 224-229
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Tidskriftsartikel (refereegranskat)abstract
- Viral persistence and autoantibodies are pathogenic components in patients with idiopathic dilated cardiomyopathy (DCM). The aim was to evaluate T-cell function in DCM using different flow cytometry based detection techniques. Following stimulation, the frequency of IFN-gamma-producing CD4+ T cells was significantly lower in patients compared with controls. In contrast, the frequency of IL-4 producing CD4+ T cells was no different. In supernatants of cultured PBMC, IFN-gamma and IL-10 were significantly lower in patients. In addition, lymphocyte proliferation was significantly lower in patients compared with controls, whereas major lymphocyte subsets were not different. IFN-gamma and IL-10 are key cytokines in the ability to mount protective immune responses and to maintain self-tolerance. A reduced activation of T-helper 1 (IFN-gamma producing) cells and a decreased capacity to produce IL-10, found in the present study, could explain parts of the autoimmune features seen in patients with DCM.
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| 30. |
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| 31. |
- Liu, Chenxiao, et al.
(författare)
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V gamma 9V delta 2 T cells proliferate in response to phosphoantigens released from erythrocytes infected with asexual and gametocyte stage Plasmodium falciparum
- 2018
-
Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749 .- 1090-2163. ; 334, s. 11-19
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Tidskriftsartikel (refereegranskat)abstract
- V gamma 9V delta 2 T cells, the dominant gamma delta T cell subset in human peripheral blood, are stimulated by phosphoantigens, of which (E)-4-Hydroxy-3-methyl-but-2-enyl pyrophosphate, is produced in the apicoplast of malaria parasites. Cell-free media from synchronised Plasmodium falciparum asexual ring, trophozoite, and schizont stage-cultures of high purity as well as media from ruptured schizont cultures, all stimulated V gamma 9V delta 2 T cell proliferation, as did media from pure gametocyte cultures, whereas media from uninfected erythrocytes cultures did not. The media from ruptured schizont cultures and all the asexual and gametocyte stage cultures contained only background iron levels, suggesting that all erythrocyte haemoglobin is consumed as the parasites develop and supporting that the phosphoantigens were released from intact parasitized erythrocytes. The V gamma 9V delta 2 T cell-stimulating agent was not affected by freezing, thawing or heating but was sensitive to phosphatase treatment, confirming its phosphoantigen identity. In summary, phosphoantigens are released from parasitised erythrocytes at all developmental blood stages.
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| 32. |
- Ohlsson, Claes, 1965, et al.
(författare)
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Regulation of bone mass by the gut microbiota is dependent on NOD1 and NOD2 signaling
- 2017
-
Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 317, s. 55-58
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Tidskriftsartikel (refereegranskat)abstract
- Germ-free (GF) mice have increased bone mass that is normalized by colonization with gut microbiota (GM) from conventionally raised (CONV-R) mice. To determine if innate immune signaling pathways mediated the effect of the GM, we studied the skeleton of GF and CONV-R mice with targeted inactivation of MYD88, NOD1 or NOD2. In contrast to WT and Myd88(-/-) mice, cortical bone thickness in mice lacking Nodi or Nod2 was not increased under GF conditions. The expression of Tnf alpha and the osteoclastogenic factor Rankl in bone was reduced in GF compared to CONV-R WT mice but not in Nodl(-/-) or Nod2(-/-) mice indicating that the effect of the GM to increase Tnfa and Rankl in bone and to reduce bone mass is dependent on both NOD1 and NOD2 signaling.
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| 33. |
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| 34. |
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| 35. |
- Pradhananga, Sailendra, et al.
(författare)
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Promoter anchored interaction landscape of THP-1 macrophages captures early immune response processes
- 2020
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749 .- 1090-2163. ; 355
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Tidskriftsartikel (refereegranskat)abstract
- Macrophages are highly plastic immune cells with temporally distinct transcriptome changes upon lipopolysaccride (LPS) activation. However, to what extent transcriptome reprogramming is mediated via spatial chromatin looping is not well studied. We generated high resolution chromatin interaction maps for LPS-stimulated THP-1 macrophages (0 and 2 h) using capture Hi-C. Success of LPS stimulation was validated with transcriptome sequencing. Circa 2900 genes changed their interaction profile upon LPS stimulation and those gaining interactions were enriched for LPS response relevant processes, suggesting a substantial role for distal regulation. Immune and cardiovascular risk variants were enriched within the interacting regions, thereby providing insights into macrophage biology.
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| 36. |
- Saeidi, Alireza, et al.
(författare)
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Concurrent loss of co-stimulatory molecules and functional cytokine secretion attributes leads to proliferative senescence of CD8(+) T cells in HIV/TB co-infection
- 2015
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Ingår i: Cellular Immunology. - : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 0008-8749 .- 1090-2163. ; 297:1, s. 19-32
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Tidskriftsartikel (refereegranskat)abstract
- The role of T-cell immunosenescence and functional CD8(+) T-cell responses in HIV/TB co-infection is unclear. We examined and correlated surrogate markers of HIV disease progression with immune activation, immunosenescence and differentiation using T-cell pools of HIV/TB co-infected, HIV-infected and healthy controls. Our investigations showed increased plasma viremia and reduced CD4/CD8 T-cell ratio in HIV/TB co-infected subjects relative to HIV-infected, and also a closer association with changes in the expression of CD38, a cyclic ADP ribose hydrolase and CD57, which were consistently expressed on late-senescent CD8(+) T cells. Up-regulation of CD57 and CD38 were directly proportional to lack of co-stimulatory markers on CD8(+) T cells, besides diminished expression of CD127 (IL-7R alpha) on CD57(+)CD4(+) T cells. Notably, intracellular IFN-gamma, perforin and granzyme B levels in HIV-specific CD8(+) T cells of HIV/TB co-infected subjects were diminished. Intracellular CD57 levels in HIV gag p24-specific CD8(+) T cells were significantly increased in HIV/TB co-infection. We suggest that HIV-TB co-infection contributes to senescence associated with chronic immune activation, which could be due to functional insufficiency of CD8(+) T cells. (C) 2015 Elsevier Inc. All rights reserved.
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| 37. |
- Saeidi, Alireza, et al.
(författare)
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Regulation of CD8+T-cell cytotoxicity in HIV-1 infection
- 2015
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Ingår i: Cellular Immunology. - : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 0008-8749 .- 1090-2163. ; 298:1-2, s. 126-133
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Forskningsöversikt (refereegranskat)abstract
- Understanding the mechanisms involved in cellular immune responses against control of human immunodeficiency virus (HIV) infection is key to development of effective immunotherapeutic strategies against viral proliferation. Clear insights into the regulation of cytotoxic CD8+ T cells is crucial to development of effective immunotherapeutic strategies due to their unique ability to eliminate virus-infected cells during the course of infection. Here, we reviewed the roles of transcription factors, co-inhibitory molecules and regulatory cytokines following HIV infection and their potential significance in regulating the cytotoxic potentials of CD8+ T cells. (C) 2015 Elsevier Inc. All rights reserved.
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| 38. |
- Sakata, Naoki, et al.
(författare)
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Differential regulation of CD40-mediated human B cell responses by antibodies directed against different CD40 epitopes
- 2000
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749 .- 1090-2163. ; 201:2, s. 109-123
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Tidskriftsartikel (refereegranskat)abstract
- Ligation of CD40 using anti-CD40 or soluble CD40-ligand activates numerous intracellular kinases which transduce signals to the nucleus. The nature whereby these signaling events are coupled to distal functional events in B cells is poorly understood. In this study, using anti-CD40 monoclonal antibodies which recognize different epitopes on CD40, we compare the ability to activate the stress-activated protein kinases (SAPK) such as c-Jun NH(2) terminal kinase and p38 in human B cells with CD40 function. Activation of the SAPK pathway correlated with levels of activation of Rel/NF-kappaB transcription factors, but did not appear to be associated with rescue from anti-IgM induced apoptosis by suppressing caspase (CPP32) activity. Somewhat surprisingly, in the presence of IL-4, those antibodies to CD40 which failed to activate SAPK were most active in IgE production. IgE production was augmented in the presence of wortmannin. These studies suggest that rescue from apoptosis and IgE production mediated via CD40 may be independent of SAPK activation, induction of Rel/NF-kappaB, or suppression of CPP32 and that IgE production is, at least in part, regulated by signaling pathways that are dependent on phosphatidylinositol 3-kinase.
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| 39. |
- Siesjö, P, et al.
(författare)
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Increased proportion of CD8+ tumor responsive T cells after immunization with tum- versus tum+ rat glioma
- 1995
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 165:2, s. 33-225
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Tidskriftsartikel (refereegranskat)abstract
- Previously established immunogenic (tum-) clones of an ENU (ethyl-N-nitrosourea)-induced rat glioma, N32, were compared to the original tumor concerning their capacity to induce T lymphocyte responses after in vivo immunization and in vitro restimulation of responder spleen cells in mixed lymphocyte tumor culture (MLTC) assays. Quite unexpectedly, original N32 (tum+) in vivo primed spleen cells proliferated to the same extent in vitro in response to tum+ stimulator cells as did tum- in vivo primed spleen cells. However, flow-cytometric analysis of parallel cultures showed a greatly increased proportion of CD3+CD8+ lymphocytes in the proliferating responder cell population from tum- immunized hosts, contrary to a CD3+CD4+ lymphocyte dominance after tum+ immunization. Although the original tum+ N32 tumor cells are not capable of inducing a clearly demonstrable isograft rejection response, they induce a strong T cell response readily detectable in MLTC assays. We propose that the increased CD8+ lymphocyte proliferation could be an essential feature of the isograft rejection response induced by tum- tumor variants. Possible mechanisms of the augmented CD8+ T cell response are discussed.
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| 40. |
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| 41. |
- Tegnér, Jesper, et al.
(författare)
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Systems biology of innate immunity
- 2006
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Ingår i: Cellular Immunology. - : Elsevier BV. - 0008-8749 .- 1090-2163. ; 244:2, s. 105-109
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Tidskriftsartikel (refereegranskat)abstract
- Systems Biology has emerged as an exciting research approach in molecular biology and functional genomics that involves a systematic use of genomic, proteomic, and metabolomic technologies for the construction of network-based models of biological processes. These endeavors, collectively referred to as systems biology establish a paradigm by which to systematically interrogate, model, and iteratively refine our knowledge of the regulatory events within a cell. Here, we present a new systems approach, integrating DNA and transcript expression information, specifically designed to identify transcriptional networks governing the macrophage immune response to lipopolysaccharide (LPS). Using this approach, we are not only able to infer a global macrophage transcriptional network, but also time-specific sub-networks that are dynamically active across the LPS response. We believe that our system biological approach could be useful for identifying other complex networks mediating immunological responses. © 2007 Elsevier Inc. All rights reserved.
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| 42. |
- Tovar Fernandez, Maria C., et al.
(författare)
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Substrate-specific presentation of MHC class I-restricted antigens via autophagy pathway
- 2022
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Ingår i: Cellular Immunology. - : Elsevier. - 0008-8749 .- 1090-2163. ; 374
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Tidskriftsartikel (refereegranskat)abstract
- The accumulation of protein aggregates is toxic and linked to different diseases such as neurodegenerative disorders, but the role of the immune system to target and destroy aggregate-carrying cells is still relatively unknown. Here we show a substrate-specific presentation of antigenic peptides to the direct MHC class I pathway via autophagy. We observed no difference in presentation of peptides derived from the viral EBNA1 protein following suppression of autophagy by knocking down Atg5 and Atg12. However, the same knock down treatment suppressed the presentation from ovalbumin. Fusing the aggregate-prone poly-glutamine (PolyQ) to the ovalbumin had no effect on antigen presentation via autophagy. Interestingly, fusing the EBNA1-derived gly-ala repeat (GAr) sequence to ovalbumin rendered the presentation Atg5/12 independent. We also demonstrate that the relative levels of protein expression did not affect autophagy-mediated antigen presentation. These data suggest a substrate-dependent presentation of antigenic peptides for the MHC class I pathway via autophagy and indicate that the GAr of the EBNA1 illustrates a novel virus-mediated mechanism for immune evasion of autophagy-dependent antigen presentation.
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| 43. |
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| 44. |
- Zhang, K, et al.
(författare)
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A MUC1 mucin secreted from a colon carcinoma cell line inhibits target cell lysis by natural killer cells.
- 1997
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Ingår i: Cellular immunology. - : Elsevier BV. - 0008-8749. ; 176:2, s. 158-65
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Tidskriftsartikel (refereegranskat)abstract
- The effect of two secreted mucin-type glycoproteins on natural killer (NK) cell cytotoxicity against K562 target cells has been studied. These mucins carry the carcinoma-associated sialyl-Lewis a carbohydrate epitopes and were purified from the human colon adenocarcinoma cell line COLO 205 secretions, where they lack their cytoplasmic parts. The larger one has an apoprotein encoded by the MUC1 gene, and the smaller one has CD43 (leukosialin) as the core protein. The purified MUC1 mucin could inhibit the target cell lysis by NK cells in a dose-response-dependent way, whereas other mucin domains of similar size showed no inhibition. The second mucin, CD43, inhibited lysis by NK cells, although less than the larger one. The MUC1 mucin bound to the enriched natural killer cell preparations in a partial Ca2+-dependent way as well. This mucin also bound to the target cells. The K562 cells, normally expressing high amount of CD43, showed an increased resistance to lysis by NK cells when transfected with MUC1 cDNA compared with nontransfected cells. One can speculate that mucins secreted or expressed in the plasma membrane of cancer cells could interfere with NK cell-mediated lysis.
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| 45. |
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