IL-33-induced keratoconjunctivitis is mediated by group 2 innate lymphoid cells in mice

Innate lymphoid cell Vernal keratoconjunctivitis Keratoconjunctivitis T helper cell
DOI: 10.1016/j.alit.2022.10.003 Publication Date: 2022-10-29T22:44:54Z
ABSTRACT
Interleukin-33 (IL-33) is involved in type 2 innate immunity by inducing cytokines, such as IL-5 and IL-13, through the activation of group lymphoid cells (ILC2s) or T helper (Th2) cells. We previously reported that mice overexpressing IL-33 (IL-33Tg) cornea conjunctiva spontaneously develop atopic keratoconjunctivitis-like inflammation. Despite previous studies, it not fully understood what types immune contribute to disease process IL-33-induced keratoconjunctivitis.To defect Th2 cells, IL-33Tg were crossed with Rag2KO mice. To ILC2s, received bone marrow transplantations from B6.C3(Cg)-Rorasg/J lacked ILC2. Immunostaining techniques used determine where ILC2 distributed conjunctiva. analyzed transcriptomes using single-cell RNA-seq analysis. investigate whether tacrolimus reduces cytokine production ILC2, was cultured tacrolimus, percentage cytokine-producing examined. can inhibit keratoconjunctivitis vivo, treated eye drops.ILC2 infiltrated conjunctival epithelium subepithelial tissue. Keratoconjunctivitis developed Rag2KO/IL-33Tg mice, but abolished lacking a uniform cluster heterogeneous cluster. Tacrolimus inhibited ILC2s vitro, drops vivo.ILC2 plays pivotal role
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