Susan L. Kalled

TL;DR: It is demonstrated that BAFF Tg mice, as they age, develop a secondary pathology reminiscent of Sjögren's syndrome, and altered B cell differentiation and tolerance induced by excess BAFF may be central to SS pathogenesis.

TL;DR: It is demonstrated that under conditions where BAFF levels are elevated, autoantigen-engaged cells will be rescued from rapid competitive elimination, predisposing to the development of autoimmune disease.

TL;DR: BAFF-R is important not only for splenic B cell maturation, but is the major mediator of BAFF-dependent costimulatory responses in peripheral B and T cells.

TL;DR: BAFF may enhance humoral immunity in vivo by promoting survival of ISCs via a BCMA-dependent mechanism and have wide-ranging implications for the treatment of human immunodeficiencies as well as autoimmune diseases.

TL;DR: A soluble form of BCMA, which inhibited the binding of BAFF to a B cell line, induced a dramatic decrease in the number of peripheral B cells when administered in vivo, consistent with a role for BAFF in maintaining homeostasis of the B cell population.