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Cbl‐b differentially regulates activation‐induced apoptosis in T helper 1 and T helper 2 cells
Author(s) -
Hanlon Allison,
Jang Sihyug,
Salgame Padmini
Publication year - 2005
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2005.02252.x
Subject(s) - apoptosis , microbiology and biotechnology , cd3 , lipid raft , biology , t cell , ligation , cytotoxic t cell , chemistry , signal transduction , immunology , antigen , immune system , in vitro , biochemistry , cd8
Summary We previously reported that ligation of CD3 induces antiapoptotic signals in T helper 2 (Th2) cells, and in contrast causes Th1 cells to undergo apoptosis. Here we show that Cbl‐b is accountable for the unequal response, revealing a previously unknown cell‐specific regulatory function for the molecule. Absence of Cbl‐b resulted in resistance to activation‐induced apoptosis in murine Th1 cells following CD3 ligation, akin to what is observed in Th2 cells containing Cbl‐b. Concurrent with the apoptosis profile, CD3 ligation in the absence of Cbl‐b induced raft mobilization and cytoskeletal rearrangement in Th1 cells. Despite their ability to signal from CD3, Th2 cells did not aggregate their rafts, providing an explanation for cell‐specific activity of Cbl‐b.