Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 45, Issue 2, Pages 513-524Publisher
WILEY-BLACKWELL
DOI: 10.1002/eji.201444744
Keywords
Bacterial infection; CARD9; CD4(+) T cells; Syk; TLRs
Categories
Funding
- National Institutes of Health [AI076278, AI055743]
- MRC [U117527252]
- Medical Research Council [MC_U117527252] Funding Source: researchfish
- The Francis Crick Institute [10194] Funding Source: researchfish
- MRC [MC_U117527252] Funding Source: UKRI
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Toll-like receptors (TLRs) can recognize microbial patterns and utilize adaptor molecules, such as-MyD88 or (TRIF TIR-domain-containing adapter-inducing interferon-beta), to initiate downstream signaling that ultimately affects the initiation of adaptive immunity. In addition to this inflammatory role, TLR5 expression on dendritic cells can favor antigen presentation of flagellin peptides and thus increase the sensitivity of flagellin-specific T-cell responses in vitro and in vivo. Here, we examined the role of alternative signaling pathways that might regulate flagellin antigen presentation in addition to MyD88. These studies suggest a requirement for spleen tyrosine kinase, a noncanonical TLR-signaling adaptor molecule, and its downstream molecule CARD9 in regulating the sensitivity of flagellin-specific CD4(+) T-cell responses in vitro and in vivo. Thus, a previously unappreciated signaling pathway plays an important role in regulating the dominance of flagellin-specific T-cell responses.
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