| First Author | Krawczyk C | Year | 2000 |
| Journal | Immunity | Volume | 13 |
| Issue | 4 | Pages | 463-73 |
| PubMed ID | 11070165 | Mgi Jnum | J:79550 |
| Mgi Id | MGI:2388463 | Doi | 10.1016/s1074-7613(00)00046-7 |
| Citation | Krawczyk C, et al. (2000) Cbl-b is a negative regulator of receptor clustering and raft aggregation in T cells. Immunity 13(4):463-73 |
| abstractText | Stimulation of T cells via the antigen and costimulatory receptors leads to the organization of a supramolecular activation cluster called the immune synapse. We report that loss of the molecular adaptor Cbl-b in T cells frees antigen receptor-triggered receptor clustering, lipid raft aggregation, and sustained tyrosine phosphorylation from the requirement for CD28 costimulation. Introduction of the cbl-b mutation into a vav1-/- background relieved the functional defects of vav1-/- T cells and caused spontaneous autoimmunity. Wiscott Aldrich Syndrome protein (WASP) was found to be essential for deregulated proliferation and membrane receptor reorganization of cbl-b mutant T cells. Antigen receptor-triggered Ca2+ mobilization, cytokine production, and receptor clustering can be genetically uncoupled in cbl-b mutant T cells. Thus, Cbl-b functions as a negative regulator of receptor clustering and raft aggregation in T cells. |
