免疫学
先天性淋巴细胞
固有层
免疫系统
T细胞
嗜酸性粒细胞
调节性T细胞
生物
上皮内淋巴细胞
特应性皮炎
免疫
白细胞介素2受体
上皮
遗传学
哮喘
作者
Tingting Wang,Qiao Wang,Yang Xie,Jingchang Ma,Wei Hu,Yang Lu,Xuemei Li,Chujun Duan,Shihao Wu,Yuling Wang,Kun Cheng,Yuan Zhang,Ran Zhuang
出处
期刊:Immunology
[Wiley]
日期:2023-03-20
卷期号:169 (4): 431-446
摘要
Abstract Intestinal mucosal immunity plays a pivotal role in host defence. In this study, we found that cluster of differentiation 226 (CD226) gene knockout (KO) led to more severe atopic dermatitis (AD)‐related skin pathologies and bowel abnormalities in a 2,4‐dinitrochlorobenzene (DNCB)‐induced AD‐like mouse model. Following DNCB administration, the expression of CD226 was elevated in intestinal mucosal tissues, including group 3 innate lymphoid cells (ILC3s) and CD4 + T cells of Peyer's patches (PPs). CD226 deficiency led to an overactive intestinal immune response in the AD‐like mice, as evidenced by increased inflammation and Th1/Th2‐related cytokine levels as well as increased Paneth cell numbers and antimicrobial peptide (AMP) expression, which was likely due to the higher interleukin (IL)‐22 production in the lamina propria. Additionally, CD226 deficiency increased the production of IL‐4 and IL‐17 in mesenteric lymph nodes as well as the number of PPs and expression of immunoglobulin (Ig) A in B cells. Moreover, insufficient expression of CD226 affected the characterization of intraepithelial and lamina propria lymphocytes in the intestinal mucosa. Finally, the number of PPs was increased in CD4 + T cell‐specific CD226 KO and regulatory T (Treg) cell‐specific CD226 KO mice; thus, loss of CD226 in Treg cells resulted in impaired Treg cell‐suppressive function. Therefore, our findings indicate that CD226 deficiency alters intestinal immune functionality in inflammatory diseases.
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