期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 115, 期 2, 页码 459-467出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200522462
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资金
- NHLBI NIH HHS [R01 HL054450, HL56389, HL54450, P50 HL056389, P01 HL056389] Funding Source: Medline
- NIGMS NIH HHS [5 T32 GM07205, T32 GM007205] Funding Source: Medline
MyD88 is a common Toll-like receptor (TLR) adaptor molecule found to be essential for induction of adaptive Th1 immunity. Conversely, innate control of adaptive Th2 immunity has been shown to occur in a MyD88-independent manner. In this study, we show that MyD88 is an essential innate component in the induction of TLR4-dependent Th2 responses to intranasal antigen; thus we demonstrate what we believe to be a novel role for MyD88 in pulmonary Th2 immunity. Induction of the MyD88-independent type I IFN response to LPS is defective in the pulmonary environment. Moreover, in the absence of MyD88, LPS-induced upregulation of costimulatory molecule expression on pulmonary DCs is defective, in contrast to what has been observed with bone marrow-derived DCs (BMDCs). Reconstitution of Th2 responses occurs upon adoptive pulmonary transfer of activated BMDCs to MyD88-deficient recipients. Furthermore, the dependence of Th2 responses on MyD88 is governed by the initial route of antigen exposure; this demonstrates what we believe are novel site-specific innate mechanisms for control of adaptive Th2 immunity.
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