Molecular mechanisms of B cell tolerance, proliferation and motility.

摘要

Chapter 1 presents our investigation on how BCR signaling is affected by self-reactivity and how the dysregulation of PIP3 generation via the loss of PTEN leads to a break in B cell tolerance. The proliferation of antigen-specific lymphocytes and resulting clonal expansion are essential for adaptive immunity. Chapter 2 discusses the impact of the loss of CD98 on immune responses, particularly on the expansion of antigen-activated B cells. B cells adhere and migrate in response to chemokines in order to function and to differentiate. The molecular events downstream of BCR, S1P and chemokine stimulation leading to integrin activation are not completely understood. In Chapters 3 and 4, the roles of SHEP1 and beta1 integrin in B cells are investigated. Finally, Chapter 5 presents a research proposal on the role of the inflammasome in the pathogenesis of gout, which was written during my clinical experience in Rheumatology as a Howard Hughes Med-Into-Grad Scholar.