Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function.
摘要：
MyD88, originally isolated as a myeloid differentiation primary response gene, is shown to act as an adaptor in interleukin-1 (IL-1) signaling by interacting with both the IL-1 receptor complex and IL-1 receptor-associated kinase (IRAK). Mice generated by gene targeting to lack MyD88 have defects in T cell proliferation as well as induction of acute phase proteins and cytokines in response to IL-1. Increases in interferon-gamma production and natural killer cell activity in response to IL-18 are abrogated. In vivo Th1 response is also impaired. Furthermore, IL-18-induced activation of NF-kappaB and c-Jun N-terminal kinase (JNK) is blocked in MyD88-/- Th1-developing cells. Taken together, these results demonstrate that MyD88 is a critical component in the signaling cascade that is mediated by IL-1 receptor as well as IL-18 receptor.
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关键词：
Animals Mice, Inbred C57BL Mice, Knockout Humans Mice Th1 Cells Cells, Cultured COS Cells Adaptor Proteins, Signal Transducing DNA
DOI：
10.1016/S1074-7613(00)80596-8
被引量：
年份：
1998
Elsevier
BMJ
Semantic Scholar
dx.doi.org
NCBI
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