Abstract
Abstract Sensing of tissue injury through interleukin 33 (IL-33) release from damaged epithelial and endothelial cells directs effector function(s) of T helper and cytotoxic subsets, group 2 innate lymphocytes, and various myeloid cells. However, it is unclear whether noncanonical IL-33 production from conventional dendritic cells (cDC) shapes infection outcome. This study interrogated whether IL-33 from epithelial cells functioned differently from IL-33 derived from conventional dendritic cells (cDC) during helminth driven Type 2 inflammation. Data show mice temporally deleted of intestinal epithelial cell IL-33 (VillinCre-ERIL33flox/flox)failed to induce ILC2 expansion and host immunity against the hookworm parasite Nippostrongylus brasiliensis, whereas selective loss of cDC-derived IL-33 (CD11cCreIL33flox/flox) abrogated ST2+Foxp3+Treg responses, enhanced TH2 and ILC2 responses, and accelerated worm clearance. Lack of cDC intrinsic IL-33 impaired Foxp3+Treg expansion and anti-IL-2/IL-2 complex administration restored Treg numbers and suppressed worm clearance in CD11cCreIL-33flox/floxmice compared to CD11cCrecontrols. Collectively, this work emphasizes cellular source as a key determinant in the ability of IL-33 to direct pathogen-specific immunity.
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