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发布于:2021-10-10 18:38:01  访问:98 次 回复:0 篇
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Presence of bacterial DNA in several samples of bone marrow tissues
R Brownlie1, LK Myers2, VM Corrigall3, MD Bodman-Smith3, SJ order 187389-52-2 Thompson1, GS Panayi3 1Department of Immunology, School of Life Sciences, KCL, London, UK; 2Department of Paediatrics UT Medical Group Inc., Memphis, LPA2 antagonist 1 site Tennessee, USA; 3Department of Academic Rheumatology, GKT School of Warfarin site Medicine, KCL, London, UK Arthritis Res Ther 2005, 7(Suppl 1):P55 (DOI 10.1186/ar1576) Background Previously we have described the stress Carbetocin protein BiP as a putative autoantigen in RA [1]. purchase Staurosporine Results Administration i.v. or s.c. of BiP significantly reduced (P < 0.05) the incidence and severity of CIA when given at the onset of disease.Presence of bacterial DNA in several samples of bone marrow tissues isolated from RA patients. We could amplify DNA encoding bacterial 16S-ribosomal RNA in one bone marrow plasma and three BMMC out of total five analyzed samples. Conclusions Our results indicate that CpG oligodeoxynucleotides, the potent agonists of TLR9, modulate the activity of B cells from bone marrow of RA patients via induction of costimulatory and adhesion molecules (CD86, CD54) expression, and via cell proliferation. Thus, our data suggest that bone marrow of RA patients may represent an important secondary lymphoid organ that actively participates in the pathogenesis of RA.P55 BiP induces IL-4-dependent regulatory cellsConclusion These data indicate IL-17 to be an important upstream proinflammatory cytokine driving joint pathology during flare-up of experimental arthritis and suggest therapeutic benefit of neutralizing IL-17 during relapses of rheumatoid arthritis. R Brownlie1, LK Myers2, VM Corrigall3, MD Bodman-Smith3, SJ Thompson1, GS Panayi3 1Department of Immunology, School of Life Sciences, KCL, London, UK; 2Department of Paediatrics UT Medical Group Inc., Memphis, Tennessee, USA; 3Department of Academic Rheumatology, GKT School of Medicine, KCL, London, UK Arthritis Res Ther 2005, 7(Suppl 1):P55 (DOI 10.1186/ar1576) Background Previously we have described the stress protein BiP as a putative autoantigen in RA [1]. The administration of BiP intravenously (i.v.) prior to induction of collagen-induced arthritis (CIA) resulted in almost complete amelioration of disease [1]. Our studies now indicate that BiP has several immunomodulatory actions including the skewing of T-cell differentiation towards Th2 [2]. Aim This study focused on the therapy of CIA and investigated subcutaneous administration of BiP in comparison with intravenous administration and whether adoptive transfer of BiP-treated cells could successfully inhibit the onset of disease. Finally, IL-4 knockout mice were used to determine the importance of the T cell in the therapeutic role of BiP Methods CIA was induced in DBA-1 mice by injection of bovine collagen type II (CII) in complete Freund‘s adjuvant followed by a booster injection in incomplete Freund‘s adjuvant at day 21. At the first appearance of swollen joints, the mice were injected subcutaneously (s.c.) with BiP, a control protein, BSA or vehicle control (PBS). Disease progression was followed by measurement of swollen joints. At termination, splenocytes and draining lymph node cells were removed and T-cell cytokine secretion was assessed. Mixed spleens and lymph nodes from groups of DBA-1 PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/10382858 mice that had been immunized s.c.
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