LAT regulates γδ T cell homeostasis and differentiation

被引:96
作者
Nuñez-Cruz, S
Aguado, E
Richelme, S
Chetaille, B
Mura, AM
Richelme, M
Pouyet, L
Jouvin-Marche, E
Xerri, L
Malissen, B
Malissen, M
机构
[1] Univ Mediterranee, Ctr Immunol Marseille Luminy, CNRS, INSERM, F-13288 Marseille 9, France
[2] Inst J Paoli I Calmettes, F-13009 Marseille 9, France
[3] Univ Grenoble 1, INSERM, U548, Commissariat Energie Atom,Lab Immunochim, F-38054 Grenoble 9, France
关键词
D O I
10.1038/ni977
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
LAT (linker for activation of T cells) is essential for T cell receptor signaling. Mice homozygous for a mutation of the three C-terminal LAT tyrosine residues showed a block in alphabeta T cell development and a partially impaired gammadelta T cell development. Without intentional immunization, they accumulated gammadelta T cells in the spleen and lymph nodes that chronically produced T helper type 2 cytokines in large amounts, and caused the maturation of plasma cells secreting immunoglobulin E (IgE) and IgG1. These effects are very similar to that triggered in the alphabeta lineage by a mutation involving a distinct LAT tyrosine. Thus, LAT is an essential regulator of T cell homeostasis and terminal differentiation.
引用
收藏
页码:999 / 1008
页数:10
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