A B cell explanation for autoimmune disease: Or where is the end of a ball of string? 
(Seminars)
20 March 2012
3.30pm
Venue: Room 501.505, Level 5, Building 501, Faculty of Medical and Health Sciences, Grafton Campus
Contact info: Robyn McDonald
Contact email: r.mcdonald@auckland.ac.nz
Department of Molecular Medicine and Pathology seminar by Professor Fiona McQueen.
More than 60 years ago, Burnet and Mackay first proposed the “forbidden clone” hypothesis, postulating that autoimmune disease arises as a result of persistence of self-reactive clones of lymphocytes that should have been deleted via immune tolerance. These autoreactive clones could effect immune-mediated end-organ damage via peripheral self-antigen recognition. Recent evidence that stretches across the boundaries of many medical specialties supports this proposal, implicating a B cell precursor as the culprit. The success of B cell depleting therapy, detection of autoantibodies years before disease-onset and findings of B cell and plasma cell clonality in many autoimmune conditions will be discussed.
