β-Defensins: Linking Innate and Adaptive Immunity Through Dendritic and T Cell CCR6

TLDR

Defensins defend hosts by disrupting microbial cytoplasmic membranes. The study demonstrates that human β‑defensins attract immature dendritic cells and memory T cells. β‑defensins selectively chemotax CCR6‑expressing dendritic and memory T cells, a response blocked by pertussis toxin or anti‑CCR6 antibodies and competing with LARC binding, indicating they recruit these cells to infection sites.

Abstract

Defensins contribute to host defense by disrupting the cytoplasmic membrane of microorganisms. This report shows that human β-defensins are also chemotactic for immature dendritic cells and memory T cells. Human β-defensin was selectively chemotactic for cells stably transfected to express human CCR6, a chemokine receptor preferentially expressed by immature dendritic cells and memory T cells. The β-defensin–induced chemotaxis was sensitive to pertussis toxin and inhibited by antibodies to CCR6. The binding of iodinated LARC, the chemokine ligand for CCR6, to CCR6-transfected cells was competitively displaced by β-defensin. Thus, β-defensins may promote adaptive immune responses by recruiting dendritic and T cells to the site of microbial invasion through interaction with CCR6.