ena-STUDY-DRFZ-23-09-2013-16:29:52:957-36
Control of microbiota by LTa produced by RORgt+ cells
Immunoglobulin A (IgA) production at mucosal surfaces contributes to protection against pathogens and controls intestinal microbiota composition. However, mechanisms regulating IgA induction are not completely defined. We show that soluble lymphotoxin a (sLTa3) produced by ROR?t+ innate lymphoid cells (ILC) controls T-cell-dependent IgA induction in the lamina propria via regulation of T cell homing to the gut. On the other hand, membrane-bound lymphotoxin ß (LTa1ß2) produced by ROR?t+ ILC is critical for T-cell-independent IgA induction in the lamina propria via control of dendritic cell functions. Ablation of LTa in ROR?t+ cells abrogated IgA production in the gut and altered microbiota composition. Thus, soluble and membrane-bound lymphotoxins produced by ILC distinctly organize adaptive immune responses in the gut and control commensal microbiota composition.
Immunoglobulin A (IgA) production at mucosal surfaces contributes to protection against pathogens and controls intestinal microbiota composition. However, mechanisms regulating IgA induction are not completely defined. We show that soluble lymphotoxin a (sLTa3) produced by ROR?t+ innate lymphoid cells (ILC) controls T-cell-dependent IgA induction in the lamina propria via regulation of T cell homing to the gut. On the other hand, membrane-bound lymphotoxin ß (LTa1ß2) produced by ROR?t+ ILC is critical for T-cell-independent IgA induction in the lamina propria via control of dendritic cell functions. Ablation of LTa in ROR?t+ cells abrogated IgA production in the gut and altered microbiota composition. Thus, soluble and membrane-bound lymphotoxins produced by ILC distinctly organize adaptive immune responses in the gut and control commensal microbiota composition.