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The ubiquitin E3 ligase Cbl-b in T cells tolerance and tumor immunity Loeser S; Penninger JMCell Cycle 2007[Oct]; 6 (20): 2478-85The implication of the immune system in tumor surveillance is proven and widely accepted. However, anti-cancer immunotherapy is still difficult due to insufficient activation, immune suppression and tolerance induction. The ubiquitin E3 ligase Cbl-b, is a member of the Cbl (casitas B-lineage lymphoma) protein family and was identified as a key dominant "tolerogenic" factor in T cells that directly regulates T-cell activation by controlling activation thresholds and the requirement for co-stimulation. Intriguingly, Cbl-b deficient mice spontaneously reject a variety of cancers including spontaneous solid tumors and hematopoietic malignancies. Mechanistically, modulation of Cbl-b in T cells controls activation of tumor-reactive cytotoxic T cells in vivo and might circumvent several limitations of T cell immunotherapy. Therefore manipulation of Cbl-b might provide us with a unique opportunity for future immune treatment of human disorders such as autoimmunity, chronic viral infections, or cancer.|Animals[MESH]|Humans[MESH]|Immune Tolerance/*immunology[MESH]|Neoplasms/*enzymology/genetics/*immunology[MESH]|Protein Binding[MESH]|Proto-Oncogene Proteins c-cbl/deficiency/genetics/*metabolism[MESH]|Signal Transduction/immunology[MESH]|T-Lymphocytes/*enzymology/*immunology[MESH] |
