Abstract:
:Despite compromised T cell antigen receptor (TCR) signaling, mice in which tyrosine 136 of the adaptor linker for activation of T cells (LAT) was constitutively mutated (Lat(Y136F) mice) accumulate CD4(+) T cells that trigger autoimmunity and inflammation. Here we show that equipping postthymic CD4(+) T cells with LATY136F molecules or rendering them deficient in LAT molecules triggers a lymphoproliferative disorder dependent on prior TCR engagement. Therefore, such disorders required neither faulty thymic T cell maturation nor LATY136F molecules. Unexpectedly, in CD4(+) T cells recently deprived of LAT, the proximal triggering module of the TCR induced a spectrum of protein tyrosine phosphorylation that largely overlapped the one observed in the presence of LAT. The fact that such LAT-independent signals result in lymphoproliferative disorders with excessive cytokine production demonstrates that LAT constitutes a key negative regulator of the triggering module and of the LAT-independent branches of the TCR signaling cassette.
journal_name
Immunityjournal_title
Immunityauthors
Mingueneau M,Roncagalli R,Grégoire C,Kissenpfennig A,Miazek A,Archambaud C,Wang Y,Perrin P,Bertosio E,Sansoni A,Richelme S,Locksley RM,Aguado E,Malissen M,Malissen Bdoi
10.1016/j.immuni.2009.05.013subject
Has Abstractpub_date
2009-08-21 00:00:00pages
197-208issue
2eissn
1074-7613issn
1097-4180pii
S1074-7613(09)00322-7journal_volume
31pub_type
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