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- W4313349775 abstract "Abstract Th17 cells are essential regulator of autoimmune diseases. It is known that antigen presenting cells including conventional dendritic cells (cDCs) play a critical role in the differentiation of Th17 cells as the supplier of several Th17-polarizing cytokines such as IL-6 and IL-23. We have previously shown that the interaction between α9 integrin (α9) and its ligands such as tenascin-C (TN-C) enhance the production of a variety of cytokines including IL-6 by fibroblasts and macrophages. To examine the in vivo significance of α9 in Th17 development, we used murine collagen-induced arthritis (CIA). We demonstrated that α9 and TN-C were expressed by cDCs in the regional lymph nodes and the interaction between α9 and TN-C promoted the production of IL-6 from cDCs. The administration of anti-α9 antibody (55A2C) before and 2 days after first immunization with typeII collagen significantly suppressed the gene expression of IL-6 and IL-23 and the generation of Th17, but not Th1 cells in regional lymph nodes at day 7. Surprisingly at day 24, Th17, but not Th1 cell was significantly accumulated in regional lymph nodes of 55A2C-treated mice due to the down-regulation of CCR6 on Th17 cells. Nevertheless, arthritis was significantly attenuated in 55A2C-treated mice. These data suggest that α9-mediated signaling contributes to the generation of functional Th17 cells through the activation of cDCs in regional lymph node." @default.
- W4313349775 created "2023-01-06" @default.
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- W4313349775 date "2010-04-01" @default.
- W4313349775 modified "2023-09-25" @default.
- W4313349775 title "Abrogation of integrin α9β1-mediated signaling skews the generation of functional Th17 cells in regional lymph nodes of arthritic mice (135.3)" @default.
- W4313349775 doi "https://doi.org/10.4049/jimmunol.184.supp.135.3" @default.
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