CARD9 versus CARMA1 in innate and adaptive immunity

被引:93
作者
Hara, Hiromitsu [1 ]
Saito, Takashi [2 ,3 ]
机构
[1] Saga Univ, Fac Med, Dept Biomol Sci, Saga 8498501, Japan
[2] RIKEN Res Ctr Allergy & Immunol, Lab Cell Signaling, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan
[3] Osaka Univ, WPI Immunol Frontier Ctr, Osaka, Japan
关键词
NF-KAPPA-B; CELL ANTIGEN RECEPTOR; COMPARATIVE GENOMIC HYBRIDIZATION; T-CELL; MARGINAL ZONE; KINASE-BETA; INDUCED PHOSPHORYLATION; SIGNAL-TRANSDUCTION; PARACASPASE MALT1; PROTEIN CARD9;
D O I
10.1016/j.it.2009.03.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Nuclear factor-kappa B (NF-kappa B) and mitogen-activated protein kinases (MAPKs) are activated upon engagement of a wide variety of immunoreceptors. Accumulating evidence has demonstrated that B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue (MALT1) are essential signaling components for NF-kappa B and MAPK activation mediated by immunoreceptor tyrosine-based activation motif (ITAM)-coupled receptors in both adaptive and innate immunity. Recent studies have revealed that two caspase-recruitment domain (CARD) family adaptor molecules, CARD-containing MAGUK protein 1 (CARMA1) and CARD9, are crucial regulators of the ITAM-mediated signaling pathway by forming a complex with BCL10-MALT1 in lymphoid and myeloid cells, respectively. Here, we describe the immune responses and the cell-type-specific regulation mechanisms for NF-kappa B and MAPK activation controlled by CARMA1 and CARD9 through innate and adaptive immunoreceptors.
引用
收藏
页码:234 / 242
页数:9
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