期刊
NATURE IMMUNOLOGY
卷 8, 期 1, 页码 57-63出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1421
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- NIEHS NIH HHS [ES04151, ES06376] Funding Source: Medline
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R37ES004151, R01ES004151, R01ES006376] Funding Source: NIH RePORTER
Mice lacking activity of the kinase MEKK1 ('Map3k1(Delta KD)' mice) have defective activation of the kinase Jnk and increased production of T helper type 2 cytokines after T cell receptor ligation. Here we show that Map3k1(Delta KD) mice had defective germinal center formation and diminished production of antibodies recognizing thymus-dependent antigens. Those defects were B cell intrinsic, as MEKK1 was necessary for CD40-mediated activation of the kinases Jnk and p38 and transcription factor c-Jun, as well as for expression of cyclin D2 and activation-induced deaminase. MEKK1 was recruited to CD40 and adaptor molecule TRAF2 after CD40 ligation, and Map3k1(Delta KD) B cells were hypoproliferative after CD40 stimulation. Our data emphasize that MEKK1 is an essential component of signaling cascades needed for thymus-dependent antigen-induced B cell proliferation and antibody production.
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