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M2-like dermis resident macrophages regulate type 1 2 circuitries with ILC2s and eosinophils to exacerbate cutaneous leishmaniasis

ABSTRACT: Tissue-resident macrophages (TRMs) are critical for tissue homeostasis/repair. We previously showed that dermal TRMs produce CCL24 which mediates their interaction with IL-4 producing eosinophils, required to maintain their M2-like properties in the TH1 environment of the Leishmania major infected skin. Here, we unveil another layer of TRM self-maintenance involving production of TSLP, an alarmin typically characterized as epithelial cell-derived. Both TSLP signaling and IL-5+ innate lymphoid cell 2 (ILC2s) were shown to maintain dermal TRM numbers and promote infection. Single cell RNA sequencing identified the dermal TRMs as the sole source of TSLP and CCL24. Generation of Ccl24-cre mice permitted specific labeling of dermal TRMs, as well as interstitial TRMs from other organs. Genetic ablation of TSLP from dermal TRMs reduced the number of dermal TRMs and ameliorated infection. Here, we show that by orchestrating localized type 2 circuitries with ILC2s and eosinophils, dermal TRMs are self-maintained as a replicative niche for L. major.

ORGANISM(S): Mus musculus

PROVIDER: GSE243853 | GEO | 2023/10/30

REPOSITORIES: GEO

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