FOXP3型
炎症
免疫学
指炎
转录组
白细胞介素2受体
功能(生物学)
生物
调节性T细胞
T细胞
银屑病
基因
细胞生物学
基因表达
遗传学
银屑病性关节炎
免疫系统
末端炎
作者
Chelisa Cardinez,Yuwei Hao,Kristy Kwong,Ainsley Davies,Morgan B. Downes,N. Roberts,Jason D. Price,Raquel A. Hernandez,Jessica Lovell,Rochna Chand,Zhi-Ping Feng,Anselm Enders,Carola G. Vinuesa,Bahar Miraghazadeh,Matthew Cook
标识
DOI:10.1038/s41467-024-45870-3
摘要
Loss-of-function mutations have provided crucial insights into the immunoregulatory actions of Foxp3+ regulatory T cells (Tregs). By contrast, we know very little about the consequences of defects that amplify aspects of Treg function or differentiation. Here we show that mice heterozygous for an Ikbkb gain-of-function mutation develop psoriasis. Doubling the gene dose (Ikbkb
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