Apoptotic cells protect mice from autoimmune inflammation by the induction of regulatory B cells

摘要: Abstract The maintenance of immune tolerance to apoptotic cells (AC) within an inflammatory milieu is vital prevent autoimmunity. To investigate this, we administered syngeneic AC i.v. into mice carrying a cohort ovalbumin (OVA)-specific transgenic T (DO11.10) along with OVA peptide and complete Freund's adjuvant, observing dramatic increase in OVA-specific IL-10 secretion. Activated splenic B responded directly AC, increasing secretion IL-10, this programming by was key inducing cell-derived IL-10. We went on ask whether are able modulate the course autoimmune-mediated, chronic inflammation. given up 1 month before clinical onset collagen-induced arthritis protected from severe joint inflammation bone destruction. Antigen-specific CD4+ again secreted significantly more associated reduced titer pathogenic anti-collagen II antibodies. Inhibition vivo reversed beneficial effects AC. Passive transfer AC-treated provided significant protection arthritis. These data demonstrate that exert profound influence adaptive response through generation CD19+ regulatory cells, which turn cytokine profile antigen-specific effector cells. apoptosis IL-10 regulation T