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Träfflista för sökning "L773:0165 2478 OR L773:1879 0542 "

Sökning: L773:0165 2478 OR L773:1879 0542

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1.
  • Ek, Sara, et al. (författare)
  • Gene expression profiling of mantle cell lymphonas
  • 2003
  • Ingår i: Immunology Letters (Abstracts of the 15th European Immunology Congress (EFIS 2003)). - 0165-2478 .- 1879-0542. ; 87:1-3, s. 01-24
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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2.
  • Fransson, Johan, et al. (författare)
  • Internalising human anti-tumor antibodies.
  • 2003
  • Ingår i: Immunology Letters (Abstracts of the 15th European Immunology Congress (EFIS 2003)). - 1879-0542 .- 0165-2478. ; 87:1-3, s. 02-34
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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4.
  • Kuraya, M, et al. (författare)
  • C3d-mediated negative and positive signals on the proliferation of human B cells separated from blood
  • 1990
  • Ingår i: Immunology Letters. - 0165-2478 .- 1879-0542. ; 26:1, s. 51-58
  • Tidskriftsartikel (refereegranskat)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. (författare)
  • Mechanisms of TGF-beta signaling in regulation of cell growth and differentiation
  • 2002
  • Ingår i: Immunology Letters. - 0165-2478 .- 1879-0542. ; 82:1-2, s. 85-91
  • Forskningsöversikt (refereegranskat)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. (författare)
  • Monoclonal antibodies against Salmonella porins : generation and characterization
  • 1992
  • Ingår i: Immunology Letters. - Amsterdam : Elsevier. - 0165-2478 .- 1879-0542. ; 33:2, s. 201-206
  • Tidskriftsartikel (refereegranskat)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- (författare)
  • Components with potential immunosuppressive activity in lipopolysaccharide of laboratory Pseudomonas aeruginosa strains
  • 2003
  • Ingår i: Immunology Letters. - 0165-2478 .- 1879-0542. ; 85:1, s. 29-33
  • Tidskriftsartikel (refereegranskat)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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10.
  • Börjesson, Andreas, et al. (författare)
  • 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
  • Ingår i: Immunology Letters. - : Elsevier BV. - 0165-2478 .- 1879-0542. ; 136:1, s. 74-79
  • Tidskriftsartikel (refereegranskat)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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