ArticleMolecular biomedicine2026
H2A.J is an epigenetic driver of IL-17-associated inflammation in T
Article in Molecular biomedicine, 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
Psoriasis is a common autoinflammatory disease driven by excessive IL-17 expression. While the pathomechanism of the disease has been revealed, epigenetic factors contributing to psoriasis are less well understood. Here, we investigated the role of the poorly studied histone variant H2A.J in psoriasis. We found that H2A.J gets overexpressed in the skin of psoriasis patients, with even non-lesional skin showing increased expression compared to the skin of healthy donors. To gain mechanistic insights, we studied mice with a global H2A.J knockout (KO) and found them to be partially protected against experimentally induced psoriasis, highlighted by reduced immune cell infiltration and less hyperkeratosis. Molecularly, psoriatic skin of H2A.J KO mice showed diminished expression of chemokines and cytokines, including CXCL1, CCL3, and IL-17A. This phenotype could partially be explained by the role of H2A.J as a key regulator of IL-17A-responsive genes in keratinocytes. Furthermore, we uncovered a T-cell-intrinsic function of H2A.J, which specifically promoted the expression of effector molecules such as Il17a and Il17f in T
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