期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 38, 期 2, 页码 400-409出版社
WILEY-BLACKWELL
DOI: 10.1002/eji.200737602
关键词
AP-1; B cells; CD40; JNK; TLR7
类别
资金
- NCI NIH HHS [R01 CA099997, R01 CA099997-01, CA 099997, R01 CA099997-08] Funding Source: Medline
- NIAID NIH HHS [R01 AI028847, R01 AI049993-01, AI 28847, AI 49993, R01 AI028847-09, R01 AI049993, R56 AI049993-10, R01 AI028847-20, R56 AI049993, R56 AI028847] Funding Source: Medline
During vaccination or infection, adaptive and innate immune receptors of B cells are engaged by microbial antigens/ligands. A better understanding of how innate and adaptive signaling pathways interact could enlighten B lymphocyte biology as well as aid immunotherapy strategies and vaccine design. To address this goal, we examined the effects of TLR stimulation on BCR and CD40-induced B cell activation. Synergistic production of IL-6 was observed in both human and mouse primary B cells stimulated through B cell antigen receptors, CD40 and TLR7, and these two receptors also cooperated independently of BCR signals. The enhanced IL-6 production was dependent upon the activity of c-Jun kinase (JNK) and cFos. Dual stimulation through CD40 and TLR7 markedly enhanced JNK activity. The increased level of active JNK in dual-stimulated cells was accompanied by an increase in the level of active AP-1 monomers cJun and cFos. The stimulation of B cells through both CD40 and TLR7 therefore enhanced the production of cytokines through increased JNK signaling and AP-1 activity. In addition, the dual stimulation increased cFos/AP-1 species in stimulated cells, effectively expanding the repertoire of AP-1 dimers as compared to singly stimulated B cells.
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