Antigen-presenting ILC3 regulate T cell–dependent IgA responses to colonic mucosal bacteria

• DOI: 10.1084/jem.20180871
• Publication Date: 2019-02-27T20:05:33Z
• Authors: Felipe Melo-Gonzalez; Hana Kammoun; Elza Evren; Emma E. Dutton; Markella Papadopo...; Barry M. Bradford; Ceylan Tanes; Fahmina Fardus-Reid; Jonathan R. Swann; Kyle Bittinger; Neil A. Mabbott; Bruce A. Vallance; Tim Willinger; David R. Withers; Matthew R. Hepworth
• Keywords: Innate lymphoid cell; Immunoglobulin A; Mesenteric lymph nodes; Mucosal immunology; Intestinal mucosa

Intestinal immune homeostasis is dependent upon tightly regulated and dynamic host interactions with the commensal microbiota. Immunoglobulin A (IgA) produced by mucosal B cells dictates composition of bacteria residing within intestine. While emerging evidence suggests majority IgA innately may be polyreactive, mucosal-dwelling species can also elicit via T cell–dependent mechanisms. However, mechanisms that modulate magnitude quality responses remain incompletely understood. Here we demonstrate group 3 innate lymphoid (ILC3) regulate steady state between follicular helper (TfH) to limit responses. ILC3 used conserved migratory cues establish residence interfollicular regions intestinal draining lymph nodes, where they act TfH cell class switching through antigen presentation. The absence ILC3-intrinsic presentation resulted in increased selective coating colonic mucosa. Together these findings implicate node resident, antigen-presenting as a critical regulatory checkpoint generation suggest maintain tissue mutualism