| 1. |
- Ek, Sara, et al.
(author)
-
Gene expression profiling of mantle cell lymphonas
- 2003
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In: Immunology Letters (Abstracts of the 15th European Immunology Congress (EFIS 2003)). - 0165-2478 .- 1879-0542. ; 87:1-3, s. 01-24
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Conference paper (other academic/artistic)
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| 2. |
- Fransson, Johan, et al.
(author)
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Internalising human anti-tumor antibodies.
- 2003
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In: Immunology Letters (Abstracts of the 15th European Immunology Congress (EFIS 2003)). - 1879-0542 .- 0165-2478. ; 87:1-3, s. 02-34
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Conference paper (other academic/artistic)
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| 3. |
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| 4. |
- Kuraya, M, et al.
(author)
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C3d-mediated negative and positive signals on the proliferation of human B cells separated from blood
- 1990
-
In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 26:1, s. 51-58
-
Journal article (peer-reviewed)abstract
- Soluble C3d applied to human blood-derived B lymphocytes inhibited anti-μ, T cell-produced growth factor, and EBV-induced DNA synthesis in serum-free culture. C3d added to the B cell cultures 1 and 2 days after the stimulus, still exerted inhibition, though with gradually diminishing efficiency.C3d, fixed on zymosan or attached to the culture wells, induced [3H]thymidine incorporation of the B cells in serum-free medium. The concentration of C3d used to coat the wells was critical, with optimal stimulatory effect of 8.3 μg/ml. These C3d molecules were shown to be denatured.Our results are in line with earlier data on B cells derived from mouse spleen and human tonsils showing that depending on the way of presentation and its amounts, the natural ligand of CR2 can exert negative or positive signals. Moreover, we demonstrate that C3d can inhibit even the proliferative stimulus of EBV.
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| 5. |
- Moustakas, Aristidis, et al.
(author)
-
Mechanisms of TGF-beta signaling in regulation of cell growth and differentiation
- 2002
-
In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 82:1-2, s. 85-91
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Research review (peer-reviewed)abstract
- Transforming growth factor beta (TGF-beta) is a secreted protein that regulates proliferation, differentiation and death of various cell types. All immune cell lineages, including B, T and dendritic cells as well as macrophages, secrete TGF-beta, which negatively regulates their proliferation, differentiation and activation by other cytokines. Thus, TGF-beta is a potent immunosuppressor and perturbation of TGF-beta signaling is linked to autoimmunity, inflammation and cancer. Regulation of cell proliferation and differentiation by TGF-beta is a topic of great basic and clinical importance. We summarize our work on the growth inhibitory pathway downstream of TGF-beta, which is triggered by receptor serine/threonine kinases at the cell surface and downstream effectors of the Smad family. Activated Smads regulate transcription of target genes, including cell cycle inhibitors such as p21, which mediate the anti-proliferative response and partially explain the tumor suppressive action of the TGF-beta pathway. We have described a molecular mechanism of regulation of the p21 gene by Smads and transcription factor Sp1. At late stages of tumor progression, TGF-beta promotes tumorigenesis via suppression of the immune system and changes in cell differentiation of epithelial tumor cells, a phenomenon termed epithelial to mesenchymal transdifferentiation (EMT). We review our work on the role of the Smad pathway in controlling EMT. In conclusion, the molecular pathways that describe the anti-proliferative and transdifferentiating effects of TGF-beta in epithelial cells have been uncovered to great molecular detail; a future challenge will be to test their generality in other systems, including the immune system.
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| 6. |
- Muthukkaruppan, V. R., et al.
(author)
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Monoclonal antibodies against Salmonella porins : generation and characterization
- 1992
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In: Immunology Letters. - Amsterdam : Elsevier. - 0165-2478 .- 1879-0542. ; 33:2, s. 201-206
-
Journal article (peer-reviewed)abstract
- Monoclonal antibodies (mAbs) were generated against porins, one of the major outer membrane proteins of Salmonella typhi. Six clones, designated MP1, MP2, MP3 (IgG2ak), MPN4, MPN6 (IgG1k) and MPN5 (IgG2bk) were characterized by enzyme immunoassay (ELISA) for their reactivity to porins from S. typhi, Salmonella paratyphi A, S. paratyphi B, S. paratyphi C, Salmonella choleraesuis, Salmonella enteritidis, Salmonella krefeld, Salmonella panama, Salmonella typhimurium, Escherichia coli B, Shigella flexneri 1b and Pseudomonas aeruginosa. All the clones positive for S. typhi porins showed varying reactivity towards several Salmonella species. However, none of them was positive for porins from other Gram-negative bacteria or for lipopolysaccharide (LPS). The affinity constant of these mAbs, except MPN4, was found to be in the higher range. Dot ELISA revealed that the mAbs recognized porins only in their native form. The results of inhibition ELISA using horseradish peroxidase (HRP)-conjugated MP1 suggest that the clones MP1, MP2, MP3, MPN5 and MPN6 secreted antibodies to identical epitope(s) of a 36-kDa peptide and MPN4 to a different epitope of a 35-kDa peptide. The possible applications of these mAbs were discussed.
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| 7. |
- Vikström, Olena, 1972-
(author)
-
Components with potential immunosuppressive activity in lipopolysaccharide of laboratory Pseudomonas aeruginosa strains
- 2003
-
In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 85:1, s. 29-33
-
Journal article (peer-reviewed)abstract
- The ability of culture filtrate (CF) of two laboratory Pseudomonas aeruginosa strains to inhibit delayed type hypersensitivity (DTH) to non-bacterial antigen in CBA mice has been studied. It was shown that intraperitoneal injection of native CF of the strains did not affect the level of DTH. However, redox treated CF expressed the immunosuppressive activity. Gel filtration of redox activated CF through Sephadex G-200 showed that CF contains three immunosuppressive components differing by their molecular weight and specificity. All components contained lipid group and O-polysaccharide chains that indicated their lipopolysaccharide (LPS) nature. These experiments show that laboratory P. aeruginosa strains have three LPS components but not all of them display the immunosuppressive activity.
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| 8. |
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| 9. |
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| 10. |
- Börjesson, Andreas, et al.
(author)
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beta-cell specific overexpression of suppressor of cytokine signalling-3 does not protect against multiple low dose streptozotocin induced type 1 diabetes in mice
- 2011
-
In: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 136:1, s. 74-79
-
Journal article (peer-reviewed)abstract
- We investigated the impact of beta-cell specific overexpression of suppressor of cytokine signalling-3 (SOCS-3) on the development of multiple low dose streptozotocin (MLDSTZ) induced Type 1 diabetes and the possible mechanisms involved. MLDSTZ treatment was administered to RIP-SOCS-3 transgenic and wild-type (wt) mice and progression of hyperglycemia monitored. Isolated islets from both strains were exposed to human IL-1 beta (25 U/ml) or a combination of human IL-1 beta (25 U/ml) and murine IFN-gamma (1000 U/ml) for 24h or 48h and we investigated the expression of IL-1 receptor antagonist (IL-1Ra) mRNA in islet cells and secretion of IL-1Ra into culture medium. MLDSTZ treatment caused gradual hyperglycemia both in the wt mice and in the transgenic mice with the latter tending to be more sensitive. In vitro experiments on wt and transgenic islets did not reveal any differences in sensitivity to damaging effects of STZ. Exposure of wt islets to 1L-1 beta or IL-1 beta + IFN-gamma seemed to lead to a failing IL-1Ra response from SOCS-3 transgenic islets. It could be that an increased expression of a possible protective molecule against beta-cell destruction may lead to a dampered response of another putative protective molecule. This may have counteracted a protective effect against MLDSTZ in SOCS-3 transgenic mice.
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| 11. |
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| 12. |
- Diab, R. A. H., et al.
(author)
-
Immunotoxicological effects of streptozotocin and alloxan: In vitro and in vivo studies
- 2015
-
In: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 163:2, s. 193-198
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Journal article (peer-reviewed)abstract
- Streptozotocin (STZ) and alloxan (ALX), widely used to induce diabetes in experimental animals, have different structures and mechanisms of action. We investigated those effects of these drugs on the immune system that might influence engraftment efficiency and graft survival in transplantation models, and their cytotoxicity on hematopoietic cell lines. We used the minimum dose to induce diabetes in a mouse, i.e. 180 mg/kg i.v. STZ and 75 mg/kg i.v. ALX. Both groups exhibited significant decrease in body weight during 4 days post-treatment as compared to controls. We found that blood glucose in ALX-injected mice increased faster than in STZ-injected mice. The total number of recovered splenocytes was lower in STZ-injected animals than in ALX-injected animals. The survival periods of rat islet grafts in recipient mice were longer and more diverse in STZ-injected recipients (7-24 days) compared to ALX-injected recipients (6-7 days). The in vitro study showed that ALX was less cytotoxic in cell lines with IC50 values of 2809, 3679 and >4000 mu g/ml for HL60, K562 and C1498 cells respectively. STZ was more toxic, especially in HL60 cells, with IC50 values of 11.7, 904 and 1024 mu g/ml for HL60, K562 and C1498 cells respectively. Furthermore, in response to concanavalin A (Con-A), splenocytes from STZ-injected mice produced higher amounts of interferon-gamma (IFN-gamma) than those from ALX-injected mice. In conclusion, STZ was more cytotoxic than ALX in vitro and in vivo. STZ caused lymphocytopenia, which may result in longer graft survival in STZ-treated animals than in AIX-treated animals. (C) 2015 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.
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| 13. |
- Gasperov, Nina Milutin, et al.
(author)
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Epigenetic activation of immune genes in cervical cancer
- 2014
-
In: Immunology Letters. - : Elsevier. - 0165-2478 .- 1879-0542. ; 162:2, s. 256-257
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Journal article (peer-reviewed)abstract
- Immune system provides us protection from infectious pathogens and tumors formation during lifetime. Cervical cancer (CC), and its cause, human papillomavirus (HPV) are both challenges for the immune system. We present here evidence of epigenetic activation of immune system genes in CC. Illumina Infinium Human Methylation 450 K BeadChip identified genes, which were all significantly hypomethylated in CC tissue versus normal tissue. The GeneMANIA computer program identified a tight network between those genes. The most strongly correlated genes based on their function are immune effectors' process (AIM2, BST2, BTN3A3, and IL12RB1) and response to virus related genes (AIM2, BST2, and IL12RB1). Thus, activation of those genes through demethylation is probably triggered by HPV oncogenes. In conclusion, the immune system of women who do not develop CC is probably activated earlier through DNA demethylation.
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| 14. |
- Hadzic, Radinka, et al.
(author)
-
alpha1-Antitrypsin inhibits Moraxella catarrhalis MID protein-induced tonsillar B cell proliferation and IL-6 release.
- 2006
-
In: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 102:2, s. 141-147
-
Journal article (peer-reviewed)abstract
- alpha 1-Antitrypsin (AAT) is a major circulating and tissues inhibitor of serine proteinases implicated in the regulation of inflammation and host defence. There is now increasing evidence that AAT may also exhibit anti-inflammatory activities independent of its protease inhibitor function. This study was undertaken to investigate the effects of native (inhibitory) and polymerized (non-inhibitory) forms of AAT on MID (Moraxella IgD binding protein)-induced human tonsillar B cell activation in vitro. We found that 0.5 mu g/ml MID induces B cell proliferation and stimulates IL-6 release (p < 0.001) relative to non-stimulated controls. Both native and polymerized AAT (0.5 mg/ml) inhibited MID-stimulated B cell proliferation in a similar manner (by 70%, p < 0.001), whereas MID-induced IL-6 release was more strongly suppressed by polymefized (9.9-fold, p < 0.001) as compared to native AAT (2.8-fold, p < 0.01). Electrophoretic analysis of cell culture media did not indicate any interaction between AAT and MID, and flow cytometry data showed no competition for the same receptor. The effects of AATs were observed whether added together with MID or 2 h after MID-addition to cell cultures. Thus, our data demonstrate that AAT inhibits MID-induced B cell activation in vitro that is unrelated to its protease inhibitory activity and is not dependent on MID binding to the cell surface.
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| 15. |
- Hadzic, Radinka, et al.
(author)
-
α1-Antitrypsin inhibits Moraxella catarrhalis MID protein-induced tonsillar B cell proliferation and IL-6 release
- 2006
-
In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 102:2, s. 141-147
-
Journal article (peer-reviewed)abstract
- α1-Antitrypsin (AAT) is a major circulating and tissues inhibitor of serine proteinases implicated in the regulation of inflammation and host defence. There is now increasing evidence that AAT may also exhibit anti-inflammatory activities independent of its protease inhibitor function. This study was undertaken to investigate the effects of native (inhibitory) and polymerized (non-inhibitory) forms of AAT on MID (Moraxella IgD binding protein)-induced human tonsillar B cell activation in vitro. We found that 0.5 μg/ml MID induces B cell proliferation and stimulates IL-6 release (p < 0.001) relative to non-stimulated controls. Both native and polymerized AAT (0.5 mg/ml) inhibited MID-stimulated B cell proliferation in a similar manner (by 70%, p < 0.001), whereas MID-induced IL-6 release was more strongly suppressed by polymerized (9.9-fold, p < 0.001) as compared to native AAT (2.8-fold, p < 0.01). Electrophoretic analysis of cell culture media did not indicate any interaction between AAT and MID, and flow cytometry data showed no competition for the same receptor. The effects of AATs were observed whether added together with MID or 2 h after MID-addition to cell cultures. Thus, our data demonstrate that AAT inhibits MID-induced B cell activation in vitro that is unrelated to its protease inhibitory activity and is not dependent on MID binding to the cell surface.
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| 16. |
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| 17. |
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| 18. |
- Holmgren, Jan, 1944, et al.
(author)
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Mucosal adjuvants and anti-infection and anti-immunopathology vaccines based on cholera toxin, cholera toxin B subunit and CpG DNA
- 2005
-
In: Immunology Letters. - : Elsevier. - 0165-2478 .- 1879-0542. ; 97:2, s. 181-8
-
Journal article (peer-reviewed)abstract
- Mucosal immunisation may be used both to protect the mucosal surfaces against infections and as a means for immunological treatment of peripheral immunopathological disorders through the induction of systemic antigen-specific tolerance ('oral tolerance'). The development of mucosal vaccines, whether for prevention of infectious diseases or for oral tolerance immunotherapy, requires efficient antigen delivery and adjuvant systems that can help to present the appropriate vaccine or immunotherapy antigens to the mucosal immune system. The most potent (but also toxic) mucosal adjuvants are cholera toxin (CT) and the closely related Escherichia coli heat-labile enterotoxin (LT), and much effort and significant progress have been made recently to generate toxicologically acceptable derivatives of these toxins with retained adjuvant activity. Among these are the non-toxic, recombinantly produced cholera toxin B-subunit (CTB). CTB is a specific protective antigen component of a widely registered oral cholera vaccine as well as a promising vector for either giving rise to mucosal anti-infective immunity or for inducing peripheral anti-inflammatory tolerance to chemically or genetically linked foreign antigens administered mucosally. CT and CTB have also recently been used as combined vectors and adjuvants for markedly promoting ex vivo dendritic cell (DC) vaccination with different antigens and also steering the immune response to the in vivo-reinfused DCs towards either broad Th1 + Th2 + CTL immunity (CT) or Th2 or tolerance (CTB). Another type of mucosal adjuvants is represented by bacterial DNA or synthetic oligodeoxynucleotides containing CpG-motifs, which especially when linked to CTB have been found to effectively stimulate both innate and adaptive mucosal immune responses. The properties and clinical potential of these different classes of adjuvants are being discussed. © 2004 Elsevier B.V. All rights reserved.
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| 19. |
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| 20. |
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| 21. |
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| 22. |
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| 23. |
- Kuraya, M, et al.
(author)
-
C3d-mediated negative and positive signals on the proliferation of human B cells separated from blood.
- 1990
-
In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 26:1, s. 51-58
-
Journal article (peer-reviewed)abstract
- Soluble C3d applied to human blood-derived B lymphocytes inhibited anti-mu, T cell-produced growth factor, and EBV-induced DNA synthesis in serum-free culture. C3d added to the B cell cultures 1 and 2 days after the stimulus, still exerted inhibition, though with gradually diminishing efficiency. C3d, fixed on zymosan or attached to the culture wells, induced [3H]thymidine incorporation of the B cells in serum-free medium. The concentration of C3d used to coat the wells was critical, with optimal stimulatory effect of 8.3 micrograms/ml. These C3d molecules were shown to be denatured. Our results are in line with earlier data on B cells derived from mouse spleen and human tonsils showing that depending on the way of presentation and its amounts, the natural ligand of CR2 can exert negative or positive signals. Moreover, we demonstrate that C3d can inhibit even the proliferative stimulus of EBV.
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| 24. |
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| 25. |
- Lindroth, Karin, et al.
(author)
-
The role of Blimp-1 in the GC reaction : Differential expression of Blimp-1 upon immunization with TD and TI antigens
- 2007
-
In: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 113:2, s. 70-75
-
Journal article (peer-reviewed)abstract
- Humoral responses against thymus-dependent (TD) antigens are characterized by Ig class switch, somatic hypermutations (SHM) and generation of memory. These processes are thought to occur in the specialized environment of the germinal center (GC). Some thymus-independent (TI) antigens, such as native dextran B512 (Dx) can also induce formation of GCs, but the responses do not undergo substantial affinity maturation or induction of memory. Immunization with TI Dx affects later TD responses against the same epitope, reducing Dx specific IgG 1. We have studied if the different outcome of the TI- and TD-induced GC reaction is due to differences in plasma cell differentiation. The transcriptional repressor B lymphocyte-induced maturation protein, Blimp- 1, was used as a marker for differentiation of plasma cells. We show that TI GCs contain Blimp- I in early and mature GCs, in contrast to TD-induced GCs which strongly express Blimp- I only in established GCs. Furthermore, the intensity of the Blimp- I staining is stronger in TI GCs. In addition, we demonstrate that in TD responses after TI priming the pattern of Blimp- I expression is a mixture of both TI and TD responses. This is novel evidence since these TD Immoral responses against Dx display a TI isotype pattern.
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| 26. |
- Ludvigsson, Johnny
(author)
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Combination therapy for preservation of beta cell function in Type 1 diabetes: New attitudes and strategies are needed!
- 2014
-
In: Immunology Letters. - : Elsevier. - 0165-2478 .- 1879-0542. ; 159:1-2, s. 30-35
-
Research review (peer-reviewed)abstract
- In several diseases where the immune system plays an important role there has been a tremendous progress in treatment efficacy during the last decades. Based on necessary basic science these improvements are results of rapid, numerous and open-minded clinical trials where pieces of positive results step by step have been added into treatment schemes. Treatment of Type 1 diabetes has certainly improved but too slowly. It has been difficult to convince the scientific community of opinions which among non-professionals have been regarded as common sense such as the value of normal blood glucose and preservation of insulin secretion. Lack of motivation to participate in clinical trials has slowed down progress, as well as too narrow views on both pathogenesis of Type 1 diabetes and how studies should be designed to test therapeutic interventions. Studies in experimental animals can create and support hypothesis for human conditions but must not delay clinical trials too long. There is already evidence enough for intervention trials where immune suppression is combined with antigen treatment, beta cell protection, anti-inflammatory treatment, and efforts to stimulate beta cell regeneration. Regimens should be elaborated and first tried in those groups of patients where response can be expected to be best, and thereafter adjusted to increase efficacy step-wise, and in broader patient categories.
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| 27. |
- Magnusson, Sofia E, et al.
(author)
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Dysregulated Fc receptor function in active rheumatoid arthritis
- 2014
-
In: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 162:1 Pt A, s. 200-206
-
Journal article (peer-reviewed)abstract
- Given the critical role of Fc gamma receptors (FcgammaR) as primary targets for autoantibody-mediated effects an important issue is how the FcgammaR pathway is affected in autoimmune disorders. Here we investigated the FcgammaR function in monocytes from rheumatoid arthritis (RA) patients in relation to immunoglobulin levels and disease activity. Peripheral blood was obtained from 30 RA patients with clinical acute joint synovitis (active RA), 28 RA patients with no clinical signs of acute joint synovitis (non-active RA) and 34 healthy controls. Prior the functional studies the monocytes were characterized of their FcgammaRI (CD64), II (CD32), IIb (CD32b) and III (CD16) expression as well as their cell surface bound IgG. The monocytic FcgammaR function was assessed by binding of human IgG1 and IgG3 immune complexes (IC) and TNF secretion in vitro. IgG anti-citrullinated peptide antibodies (ACPA) were analyzed in the plasma. We found that monocytes from active RA patients had increased levels of FcgammaRI, II and cell surface IgG concurrently with impaired FcgammaR function. This was evident by reduced IgG1-IC binding and decreased TNF secretion in response to IgG3-IC. In contrast, monocytes from non-active RA patients displayed a normal FcgammaR function and had increased FcgammaRIIb expression together with elevated FcgammaRI, II and cell surface IgG. The ACPA levels did not differ in active and non-active RA patients but correlated with the monocytic FcgammaRIII expression in the patients. In conclusion, active RA patients display a dysregulated FcgammaR function that may represent a novel phenotypic and likely pathogenetic marker for active RA. A disease and FcgammaR function controlling effect is suggested by the increased inhibitory FcgammaRIIb in non-active RA.
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| 28. |
- Motegi, Sei-Ichiro, et al.
(author)
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Essential roles of SHPS-1 in induction of contact hypersensitivity of skin.
- 2008
-
In: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 121:1, s. 52-60
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Journal article (peer-reviewed)abstract
- SHPS-1 is a transmembrane protein that binds the protein tyrosine phosphatases SHP-1 and SHP-2 and is abundant on the surface of CD11c(+) dendritic cells (DCs). We recently showed that SHPS-1 is essential for priming by DCs of CD4(+) T cells and for development of Th17 cell-mediated experimental autoimmunity. We have now further evaluated the importance of SHPS-1 and that of its ligand CD47 in contact hypersensitivity (CHS) to 2,4-dinitro-1-fluorobenzene (DNFB). Whereas the DNFB-induced CHS response was impaired in mice that express a mutant form of SHPS-1 lacking most of the cytoplasmic region, it was unaffected in CD47-deficient mice. Moreover, treatment of wild-type mice with mAbs to SHPS-1 that either block or do not block the binding of SHPS-1 to CD47 inhibited the CHS response. A mAb to CD47 had no such effect. The 2,4-dinitro-benzenesulfonic acid-induced proliferation of, and production of IFN-gamma or IL-17 by, T cells from DNFB-sensitized wild-type mice were inhibited by either mAb to SHPS-1 but not by that to CD47. In contrast, the blocking mAbs to SHPS-1, but not that to CD47, inhibited an allogeneic mixed leukocyte reaction. Both mAbs to SHPS-1, but not that to CD47, also inhibited the lipopolysaccharide- or polyinosinic-polycytidylic acid-induced production of TNF-alpha by DCs. These results suggest that SHPS-1 is essential for development of CHS, likely as a result of its positive regulation of the priming by DCs of CD4(+) T cells. However, such regulation by SHPS-1 does not appear to require its interaction with CD47.
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| 29. |
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| 30. |
- Nilsson, B, et al.
(author)
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SDS denaturation of complement factor C3 as a model for allosteric modifications occurring during C3b binding : demonstration of a profound conformational change by means of circular dichroism and quantitative immunoprecipitation.
- 1986
-
In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 13:1-2, s. 11-14
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Journal article (peer-reviewed)abstract
- The antigenic expression of bound but not fluid-phase C3b closely resembles that of sodium dodecyl sulphate (SDS) denatured C3. For this reason, denatured C3 has been used in this study as a model to characterize the conformational changes associated with bound C3b. It was shown in circular dichroism in the far UV spectrum that profound changes in the secondary structure occurred in denatured C3. Furthermore, quantitation by immunoprecipitation of the previously observed antigenic changes during denaturation demonstrated that C3 lost 2/3 of the antigens associated with native C3 whereas 1/3 were stable. The lost antigens were completely replaced by antigens that are specific for denatured and bound C3. We postulate that the binding of C3b is accompanied by a profound conformational change distinctive of that observed in fluid-phase C3b.
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| 31. |
- Nilsson, Joacim, et al.
(author)
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Differentiation-associated redox-regulation in human B cell lines from stem cell/pro-B to plasma cell
- 2004
-
In: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 94:1-2, s. 83-89
-
Journal article (peer-reviewed)abstract
- Redox-regulation of receptors and transcription factors are important for lymphocyte activation, differentiation and apoptosis. Thioredoxin (Trx) is a key redox-regulating protein and oxidative stress sensor operating in synergy with Trx-reductase and protein disulfide isomerase (PDI). The expression of Trx, PDI, and the Trx-regulated transcription-factor Pax5 were analyzed in a panel of human B cell lines and were compared with that of the Bcl-2 family proteins, also redox-controlled. The panel included representative cells from various stages: FLEB14-4 (pro-B), REH and NALM-6 (pre-B), Rael and Daudi (small mature B), U-698 and NC0467.3 (B-blasts), LP-1, U-1996, and U-266 (plasma cells). We found a significant congruence and co-variation of Trx and Bcl-2 levels in the B-lineage, with high expression levels in early stages (pro-B and pre-B) and in the late stage representing terminally-differentiated plasma cells, whereas mid-stage small resting B cells showed a very low expression. PDI increased significantly in plasma-blasts and plasma cells, indicating its importance in the highly specialized immunoglobulin assembly-machinery, including disulfide-bond isomerization. Pax5 was expressed in early and mid-stages, but was silenced in terminal stages. We conclude that the high Trx and Bcl-2-expression early and late in the B cell maturation pathway reflects a redox-strategy favoring an increased survival potential of the B cells at those stages. © 2004 Elsevier B.V. All rights reserved.
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| 32. |
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| 33. |
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| 34. |
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| 35. |
- Skoglund, Caroline, et al.
(author)
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C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood
- 2012
-
In: Immunology Letters. - Amsterdam, Netherlands : Elsevier. - 0165-2478 .- 1879-0542. ; 142:1-2, s. 28-33
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Journal article (peer-reviewed)abstract
- Blood platelets express several receptors involved in immunity (e.g. complement-, toll-like- and Fc gamma-receptors) and release inflammatory mediators. Furthermore, formation of platelet-leukocyte aggregates has an important role during inflammatory conditions such as coronary artery disease. Thus, apart from their well-known role in haemostasis, platelets are today also recognized as cells with immunomodulatory properties. We have previously reported regulatory effects of complement protein 1q (C1q) on platelet activation in experimental setups using isolated cells. In the present study we have proceeded by investigating effects of C1q on collagen-induced aggregation, production of reactive oxygen species (ROS), formation of platelet-leukocyte aggregates and levels of soluble P-selectin in whole blood. Impedance measurements showed that C1q inhibited collagen-induced aggregation whereas it potentiated the collagen-provoked production of ROS in a luminol-dependent chemiluminescence assay. The effects of C1q on aggregation and ROS-production were dependent upon platelets, as they were no longer observed in presence of the platelet (GpIIb/IIIa) inhibitor Reopro. Furthermore, the levels of soluble P-selectin were found to be lowered upon treatment with C1q prior to addition of collagen. There was also a trend towards a decreased formation of large platelet-leukocyte aggregates in collagen-stimulated whole blood following C1q treatment. In conclusion, our data indicate that C1q could have a role in regulating platelet activation and associated leukocyte recruitment during vessel wall injury. This has implications for inflammatory disorders such as coronary artery disease.
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| 36. |
- Söderlund, A, et al.
(author)
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Allergen induced cytokine profiles in type I allergic individuals before and after immunotherapy.
- 1997
-
In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 57:1-3, s. 177-81
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Journal article (peer-reviewed)abstract
- Allergen immunotherapy (IT) involves subcutaneous injections of increasing doses of specific allergen over a period of time. It is recognised as highly effective in the treatment of patients with allergic rhinitis. However, the specific immunological mechanisms by which IT achieves its effect have not been fully elucidated. Recent studies, have shown that the clinical effects following IT of allergic individuals is concomitant with a reduced production of IL-4 by allergen specific CD4+ T-cells. The aim of the present study was to gain better knowledge about the immunological mechanisms by which IT exerts its beneficial effects. For this purpose, peripheral blood mononuclear cells (PBMC) from ten individuals receiving birch allergen or placebo in an IT-study performed in a double-blind manner, were analysed for IL-4, IFN-gamma, IL-5 and IL-10 mRNA expression at the onset of the study and during the pollen season, during treatment. Both spontaneous and in vitro allergen-induced cytokine mRNA expression was analysed using reverse transcriptase-polymerase chain reaction (RT-PCR). Spontaneous expression of IL-4 mRNA could be detected in most of the allergic patients, but not in healthy donors. The IT-treated patients showed a decrease in the spontaneous expression of IL-4 mRNA during the pollen season as compared to at the onset of the study, while in patients receiving placebo the IL-4 mRNA expression increased or remained unchanged. Similar results were obtained after in vitro stimulation with allergen. This was in contrast to the results for IFN-gamma, which was readily detected in both patient groups with no significant differences between the groups at either timepoint. IL-5 was shown to be increased during the pollen season in both groups and thereby presumably not affected by allergen IT. Taken together, these observations suggest that the cytokine profiles in circulating T lymphocytes change as a consequence of allergen IT.
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| 37. |
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| 38. |
- Viau, M, et al.
(author)
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Down-modulation of the antigen receptor by a superantigen for human B cells
- 2004
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In: Immunology Letters. - : Elsevier BV. - 1879-0542 .- 0165-2478. ; 92:1-2, s. 91-96
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Conference paper (peer-reviewed)abstract
- B cell superantigens (SAgs) have been implicated in human diseases by demonstrating non-clonotypic expansion of B cells bearing certain immunoglobulin variable region genes. One possibility is that, during infection with microorganisms secreting SAgs, these potent molecules might modulate BcR expression. To test this hypothesis, we investigated the potential effects of a SAg, protein L from Peptostreptococcus magnus, on antigen B cell receptor (BcR) surface expression in vitro. Using fluorescence microscopy, we found that this SAg induced down-regulation of BcR expression. This effect was time-, dose-, and temperature-dependent, and shedding of cell surface IgM molecules into the culture supernatant was not detected. These data demonstrate that SAg-mediated down-regulation of the BcR expression occurs primarily as a result of BcR internalization. In addition, two specific inhibitors of protein tyrosine kinases were found to retard the BcR modulation on the cell surface and inhibit SAg-induced receptor internalization, showing that tyrosine phosphorylation is required for subsequent internalization of mIg-ligand complexes. The down-modulation of BcR expression may have pathological consequences in patients infected with microorganisms secreting SAgs. (C) 2003 Elsevier B.V. All rights reserved.
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| 39. |
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| 40. |
- Yefenof, E, et al.
(author)
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Ligands of CR2 do not interfere with C3 fragment fixation or enhanced NK sensitivity of Raji cells treated with human serum.
- 1989
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In: Immunology Letters. - 0165-2478 .- 1879-0542. ; 21:4, s. 303-306
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Journal article (peer-reviewed)abstract
- Raji cells activate the alternative complement pathway (ACP) and fix C3 fragments when incubated in human serum (HS). Earlier experiments have shown that CR2 molecules are involved in this phenomenon and the opsonized cells have elevated sensitivity to the lytic effect of CR3-bearing NK cells. We show here that Raji cells treated with CR2 site-specific ligands, (C3d, OKB-7 and HB-5 mAbs, and a synthetic peptide which binds to CR2) generated and bound C3 fragments after exposure to HS. The elevated lytic sensitivity of HS-treated cells was not altered by the presence of the various CR2 ligands. Thus, the membrane-bound C3 fragments are not fixed at the C3dg receptor binding site.
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| 41. |
- Zhang, Xiaoyin, et al.
(author)
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Proinflammatory S100A9 stimulates TLR4/NF-κB signaling pathways causing enhanced phagocytic capacity of microglial cells
- 2023
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In: Immunology Letters. - : Elsevier. - 0165-2478 .- 1879-0542. ; 255, s. 54-61
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Journal article (peer-reviewed)abstract
- Alzheimer's disease (AD) is the main cause of dementia, affecting the increasingly aging population. Growing evidence indicates that neuro-inflammation plays crucial roles, e.g., the association between AD risk genes with innate immune functions. In this study, we demonstrate that moderate concentrations of pro-inflammatory cytokine S100A9 regulate immune response of BV2 microglial cells, i.e., the phagocytic capacity, reflected by elevated number of 1 μm diameter Dsred-stained latex beads in the cytoplasm. In contrast, at high S100A9 concentrations, both the viability and phagocytic capacity of BV2 cells drop substantially. Furthermore, it is uncovered that S100A9 affects phagocytosis of microglia via NF-κB signaling pathways. Application of related target-specific drugs, i.e., IKK and TLR4 inhibitors, effectively suppresses BV2 cells’ immune responses. These results suggest that pro-inflammatory S100A9 activates microglial phagocytosis, and possibly contributes to the clearance of amyloidogenic species at the early stage of AD.
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| 42. |
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| 43. |
- Ohlin, M., et al.
(author)
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Epstein-Barr virus-induced transformation of human B lymphocytes : the effect of l-leucyl-l-leucine methyl ester on inhibitory T cell populations
- 1992
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In: Immunology Letters. - 0165-2478. ; 34:3, s. 221-228
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Journal article (peer-reviewed)abstract
- Epstein-Barr virus-mediated transformation of human B lymphocytes is inhibited by human T lymphocytes as well as by interferon-γ. Removal of the inhibitory cell populations is essential in order to achieve successful transformation in vitro. Cells with the capacity to inhibit outgrowth of lymphoblastoid cell lines can be removed by pretreatment of peripheral blood mononuclear cells with l-leucyl-l-leucine methyl ester. This treatment eliminates monocytes, NK-cells and a CD8+ T cell subpopulation. We now show that such treatment also has toxic effects on other human T cell populations. In addition, CD4+ and/or CD8+ lymphocytes are demonstrated to contain effector cell activities which inhibit outgrowth of EBV-transformed B cells. This inhibitory activity is abolished after treatment of peripheral blood mononuclear cells or purified CD4+ T cells with l-leucyl-l-leucine methyl ester. No evidence was found for a selective toxicity against any subset within the CD4+ or CD8+ T cell populations. However, the capacity of the treated cells, both peripheral blood mononuclear cells and purified CD4+ T lymphocytes, to produce mRNA encoding IFN-γ, a protein previously shown to downregulate outgrowth of EBV-transformed B cells, was selectively impaired. The results obtained suggest a role for CD4+ T cells to inhibit EBV-induced transformation of B cells.
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| 44. |
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