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The role of the CTLA-4 pathway in autoimmunity- lessons from the clinicApr 03, 2017 (Mon) | 1:00 PM -2:00 PM
Beckman Ctr, Munzer Auditorium
: Stanford, CA
CTLA-4 is involved in the function of regulatory T cells and maintains a critical immune checkpoint restraining T cell activation. Mice lacking CTLA-4 die soon after birth of profound lymphoproliferation and fatal autoimmunity and individuals treated with anti-CTLA-4 antibodies develop autoimmune side effects. Recently individuals with heterozygous (autosomal dominant) mutations in CTLA-4 have been reported who suffer from an immune dysregulation syndrome with wide ranging autoimmune features. In many cases these patients are identified as having immunodeficiency due to additional B cell defects. Despite clear evidence for their importance, the functional impact of an increasingly large number of identified mutations is not understood. We cloned and expressed CTLA-4 proteins containing a Department: Institute for Immunity, Transplantation and Infection Contact: Michele King | 650 723 3084 | mking@stanford.edu Presenter(s):
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