Induction of T helper type 2 immunity by a point mutation in the LAT adaptor |
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Authors: | Aguado Enrique Richelme Sylvie Nuñez-Cruz Selene Miazek Arkadiusz Mura Anne-Marie Richelme Mireille Guo Xiao-Jun Sainty Danielle He Hai-Tao Malissen Bernard Malissen Marie |
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Affiliation: | Centre d'Immunologie de Marseille-Luminy, INSERM- and CNRS-Université de la Méditerranée, Parc Scientifique de Luminy, 13288 Marseille Cedex 9, France. |
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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. |
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