Marcel Batten

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 IL-27Rα-deficient mice were hypersusceptible to experimental autoimmune encephalomyelitis and generated more IL-17-producing T helper cells and suppressed IL-6-mediated T cell proliferation, providing a mechanistic explanation for theIL-27-mediated immune suppression noted in several in vivo models of inflammation.

TL;DR: A model in which excessive BAFF-mediated survival of peripheral immature B cells contributes to the emergence and maturation of autoreactive B cells, skewed towards the MZ compartment is supported, providing new clues on mechanisms regulating B cell maturation and tolerance.

TL;DR: A specialized role for CxCR7 in endothelial biology and valve development is revealed and the distinct developmental role of evolutionary conserved chemokine receptors such as CXCR7 and CX CR4 is highlighted.

TL;DR: Unraveling the cellular and molecular requirements underlying Tfh cell formation and maintenance will help to identify molecules that could be targeted for the treatment of immunological diseases that are characterized by insufficient or excessive Ab responses.