| First Author | Linnemann L | Year | 2024 |
| Journal | Mucosal Immunol | PubMed ID | 39581231 |
| Mgi Jnum | J:360164 | Mgi Id | MGI:7787206 |
| Doi | 10.1016/j.mucimm.2024.11.005 | Citation | Linnemann L, et al. (2024) The C-type lectin receptor MINCLE interferes with eosinophil function and protective intestinal immunity in Strongyloides ratti-infected mice. Mucosal Immunol |
| abstractText | Strongyloides ratti is a helminth parasite that displays tissue-migrating and intestinal life stages. Myeloid C-type lectin receptors (CLRs) are pattern recognition receptors that recognize pathogen-derived ligands and initiate immune responses. To date, the role of CLRs in S. ratti infection has not been investigated. Here, we show that S. ratti-derived ligands are recognized by the CLR Macrophage inducible Ca(2+)-dependent lectin receptor (MINCLE). While MINCLE-deficiency did not affect initiation of a protective anti-S. ratti type 2 immunity, MINCLE-deficient mice had a transient advantage in intestinal immunity. Unravelling the underlying mechanism, we show that next to macrophages, dendritic cells and neutrophils, a fraction of eosinophils express MINCLE and expand during S. ratti infection. MINCLE-deficient eosinophils exhibited a more active phenotype and prolonged expansion in vivo and displayed increased capacity to reduce S. ratti motility and produce reactive oxygen species in vitro, compared to wild-type (WT) eosinophils. Depletion of eosinophils in S. ratti-infected mice after the tissue-migration phase elevated intestinal worm burden in MINCLE-deficient mice to the WT level. Thus, our findings establish a central contribution of eosinophils to parasite ejection from the intestine and suggest that S. ratti-triggered signalling via MINCLE interferes with eosinophil mediated ejection of S. ratti from the intestine. |
