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. 1998 Jul;9(1):143-50.
doi: 10.1016/s1074-7613(00)80596-8.

Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function

O Adachi  1 , T Kawai, K Takeda, M Matsumoto, H Tsutsui, M Sakagami, K Nakanishi, S Akira
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Free article

Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function

O Adachi et al. Immunity. 1998 Jul.
Free article

Abstract

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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