Abstract
Cbl-b is a member of the Cbl family of RING finger E3 ubiquitin ligases and polymorphisms and mutations in Cbl-b are associated with several autoimmune/inflammatory diseases in humans. Furthermore, gene targeting experiments in mice have provided proof of the in vivo effects of Cbl-b on T cell function and its involvement with these diseases. This brief review updates our understanding of Cbl-b in T cell tolerance, proallergic T cell development, and cancer immunity in light of the most recent advances, and their impact on autoimmune-/inflammatory diseases and cancer immunotherapy.
Highlights
Protein ubiquitination is one of fundamental regulatory post-translational modifications regulating intracellular signaling and plays potent roles in regulating a variety of signals in both innate and adaptive immune cells
Cbl-b is the only member of the Cbl family which has been documented to be crucial for T cell tolerance
We summarize the major work that we and others have carried out investigating Cbl-b in T cell tolerance and autoimmunity, proallergic T cell development, and cancer immunity
Summary
Protein ubiquitination is one of fundamental regulatory post-translational modifications regulating intracellular signaling and plays potent roles in regulating a variety of signals in both innate and adaptive immune cells. We summarize the major work that we and others have carried out investigating Cbl-b in T cell tolerance and autoimmunity, proallergic T cell development, and cancer immunity. Both groups found that Cblb−/− mice are highly susceptible to autoimmunity [3, 4], suggests that Cbl-b plays a crucial in T cell tolerance induction.
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