ArticleScience advances2026
SHARPIN restrains IL-33 release by stromal cells to control ILC2 inflammation.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Loss of SHARPIN, a component of the linear ubiquitin chain assembly complex (LUBAC), causes systemic inflammation including the accumulation of eosinophils across multiple tissues in mice. However, the mechanisms by which SHARPIN regulates type 2 inflammation remain unclear. Here, we found that SHARPIN deficiency resulted in increased numbers of type 2 innate lymphoid cells (ILC2s) in the lung and other tissues via a cell-extrinsic mechanism. SHARPIN loss enhanced interleukin-33 (IL-33) production by lung stromal cells in vivo and in vitro, thereby promoting ILC2 proliferation. Mechanistically, SHARPIN directly bound IL-33 through its Pleckstrin homology-linker region and restrained IL-33 release independently of its ubiquitination. Combined deficiency of SHARPIN and IL-33 completely reversed ILC2 increase and lung inflammation, but not stromal cell death. Our study reveals a non-canonical, ubiquitin-independent function of SHARPIN as a gatekeeper of IL-33-driven type 2 inflammation.
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