Induction of T Helper Type 2 Immunity by a Point Mutation in the LAT Adaptor

Author:

Aguado Enrique1,Richelme Sylvie1,Nuñez-Cruz Selene1,Miazek Arkadiusz1,Mura Anne-Marie1,Richelme Mireille1,Guo Xiao-Jun1,Sainty Danielle2,He Hai-Tao1,Malissen Bernard1,Malissen Marie1

Affiliation:

1. Centre d'Immunologie de Marseille-Luminy, INSERM– and CNRS–Université de la Méditerranée, Parc Scientifique de Luminy, 13288 Marseille Cedex 9, France.

2. Department of Biology, Institut Paoli-Calmettes, 232 Boulevard Sainte Marguerite, 13009 Marseille, France.

Abstract

The transmembrane protein LAT (linker for activation of T cells) couples the T cell receptor (TCR) to downstream signaling effectors. Mice homozygous for a mutation of a single LAT tyrosine residue showed impeded T cell development. However, later they accumulated polyclonal helper T (T H ) cells that chronically produced type 2 cytokines in large amounts. This exaggerated T H 2 differentiation caused tissue eosinophilia and massive maturation of plasma cells secreting to immunoglobulins of the E and G1 isotypes. This paradoxical phenotype establishes an unanticipated inhibitory function for LAT that is critical for the differentiation and homeostasis of T H cells.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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