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- W100739639 abstract "Collagen-induced arthritis can be elicited in resistant C57BL/6 mice by increasing the amount of adjuvant (dessicated Mycobacterium tuberculosis) during immunization. This adjuvant contains ligands for toll-like receptors (TLRs), especially TLR2 and TLR9, which are known to be critical for innate immune responses and are expressed on Antigen Presenting Cells (APCs) such as dendritic cells and B-cells. Our current studies are aimed at elucidating mechanisms by which TLR signaling may promote arthritis. We investigate how cross-linking TLR2 and TLR9 receptors might promote pathogenic Th-17 cells by regulating the production of IL-6 by these APCs. We isolated bone-marrow derived dendritic cells (BM-DCs) and splenic B-cells from wild type, TLR2 and TLR9 deficient B6 mice. Wild type BM-DCs produce IL-6 in response to TLR2, TLR4, and TLR9 cross-linking. Immune (but not naïve) B-cells make IL-6 in response to TLR2, TLR4 and TLR9 ligands. As compared to B6 wt, however, TLR2-KO derived DCs produced several fold more IL-6 when stimulated with TLR4 or TLR9 ligands and TLR9-KO derived DCs produced several fold more IL-6 when stimulated with TLR4 or TLR2 ligands. These findings suggest that DCs and B-cells are potent cellular sources of IL-6. IL-6 production in response to adjuvants appears to be regulated by the coordinated input of TLR signaling and may be important in the generation of pathogenic Th-17 cells." @default.
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- W100739639 date "2008-03-01" @default.
- W100739639 modified "2023-09-26" @default.
- W100739639 title "Toll‐like receptor control of IL‐6 production by dendritic cells and B cells" @default.
- W100739639 doi "https://doi.org/10.1096/fasebj.22.1_supplement.668.10" @default.
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