IL-10-producing innate lymphoid cells restrain γδT17-driven psoriatic inflammation.

Authors

Min Geun Jo, Min Yeong Choi, Keun Young Min, Jeong Won Park, Juhyun Shin, Ji-Ae Lee, Sunsook Hwang, Geunwoong Noh, Young Mi Kim, Wahn Soo Choi, Hyuk Soon Kim

Published in

iScience. Volume 29. Issue 8. Pages 117026. Aug 21, 2026. Epub Jul 31, 2026.

Abstract

Psoriasis is a chronic inflammatory dermatosis driven by the interleukin (IL)-23-IL-17 axis, with γδ T cells as key IL-17A producers in lesional skin. IL-10 counter-regulates this pathway, and innate lymphoid cells (ILCs) are emerging tissue-resident immune regulators. Here we show that imiquimod (IMQ)-induced psoriatic inflammation elicits a programmed death-ligand 1 (PD-L1)^hi stem cell antigen-1 (Sca-1)⁺ ILC2-like subset enriched for IL-10 (ILC2₁₀) that acts as an innate brake on the γδ T17 axis. Adoptive transfer of ILC2₁₀ reduced clinical severity and epidermal hyperplasia and suppressed γδ T cell IL-17A production and CCR2 expression in coculture; Il10 ^-/--derived ILC2₁₀ lacked these effects, indicating that IL-10 is required. Reanalysis of human psoriasis single-cell RNA sequencing datasets identified a PD-L1⁺IL-10⁺ ILC population in lesional skin. These findings define ILC2₁₀ as an IL-10-dependent innate regulatory checkpoint restraining γδ T17-driven psoriatic inflammation, revealing a previously unrecognized innate regulatory layer in this disease.

PMID:
42572615
Bibliographic data and abstract were imported from PubMed on 10 Aug 2026.

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