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

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Science  14 Jun 2002:
Vol. 296, Issue 5575, pp. 2036-2040
DOI: 10.1126/science.1069057

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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 (TH) cells that chronically produced type 2 cytokines in large amounts. This exaggerated TH2 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 TH cells.

  • * On leave from Institut Méditerranéen de Recherche en Nutrition, UMR-INRA, Marseille, France.

  • To whom correspondence should be addressed. E-mail: bernardm{at}ciml.univ-mrs.fr

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