Nature Immunology
4, 999 - 1008 (2003)
Published online: 14 September 2003; | doi:10.1038/ni977
LAT regulates   T cell homeostasis and differentiationSelene Nuñez-Cruz1, 5, Enrique Aguado1, 4, 5, Sylvie Richelme1, 5, Bruno Chetaille1, 2, Anne-Marie Mura1, Mireille Richelme1, Laurent Pouyet1, Evelyne Jouvin-Marche3, Luc Xerri2, Bernard Malissen1
& Marie Malissen11
Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale-Centre National de la Recherche Scientifique-Université de la Méditerranée, Parc Scientifique de Luminy, Case 906, 13288 Marseille Cedex 9, France. 2
Institut Paoli-Calmettes, 232 Boulevard Sainte Marguerite, 13009 Marseille Cedex 9, France. 3
Laboratoire d'Immunochimie, Commissariat à l'énergie atomique, Institut National de la Santé et de la Recherche Médicale, Unité 548, Université Joseph Fourier, 38054 Grenoble Cedex 9, France. 4
Present address: Department of Biochemistry and Immunology, Faculty of Medicine, University of Murcia, 30100 Murcia, Spain. 5
These authors contributed equally to this work.
Correspondence should be addressed to Bernard Malissen bernardm@ciml.univ-mrs.frLAT (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   T cell development and a partially impaired   T cell development. Without intentional immunization, they accumulated 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 lineage by a mutation involving a distinct LAT tyrosine. Thus, LAT is an essential regulator of T cell homeostasis and terminal differentiation.
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