• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

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

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.

Pubmed ID: 9697844

Authors

  • Adachi O
  • Kawai T
  • Takeda K
  • Matsumoto M
  • Tsutsui H
  • Sakagami M
  • Nakanishi K
  • Akira S

Journal

Immunity

Publication Data

July 1, 1998

Associated Grants

None

Mesh Terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Antigens, Differentiation
  • COS Cells
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Cells, Cultured
  • Cytokines
  • DNA
  • Enzyme Activation
  • Female
  • Gene Targeting
  • Humans
  • Interleukin-1
  • Interleukin-18
  • JNK Mitogen-Activated Protein Kinases
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mitogen-Activated Protein Kinases
  • Myeloid Differentiation Factor 88
  • NF-kappa B
  • Proteins
  • Receptors, Immunologic
  • Th1 Cells