Department of Pathology and Laboratory Medicine, University of Calgary, and Calgary Laboratory Services, Calgary, Alberta, Canada.
Division of Gastroenterology, University of Calgary, Calgary, Alberta, Canada.
J Crohns Colitis. 2018 Nov 28;12(12):1448-1458. doi: 10.1093/ecco-jcc/jjy116.
Inflammatory bowel disease [IBD] results particularly from an aberrance of CD4+ helper and regulatory T cells and comprises histopathologically chronic active enterocolitis with features reflecting both activity and chronicity of mucosal inflammation. The exact immunological-histological correlation in IBD is not understood.
We studied the correlation between colonic mucosal CD4+ T cell subsets [Th1, Th2, Th17, Th22 and Treg] and mucosal histological changes in ulcerative colitis [UC] and Crohn's disease [CD]. CD4+ T cell subtyping and enumeration were achieved by flow cytometry. Histological features were categorized and assessed semi-quantitatively using three validated histological scoring schemes [ECAP, RHI and D'Haens]. Correlations between prevalence [%] of CD4+ T cell subsets and histological scores were analysed.
Treg cells were correlated with ECAP category A [activity] as well as RHI scores. Treg cell were increased particularly in mucosa with severe neutrophilic infiltration in the cryptal/surface epithelium and in lamina propria, and with basal plasmacytosis. Th17 cells were also increased in cases with extensive neutrophil infiltrate in lamina propria, whereas RORc+ cells were increased in cases with severe lymphoplasmacytic infiltration in lamina propria. In both UC and CD, mucosa with marked crypt architectural alteration had increased IL-22+ and Th22 cells. UC with Paneth cell metaplasia had higher Th17 cells. CD with granuloma had increased IL-22+ and IL-22+IFN-γ+ cells.
The Treg subset appears to be associated with the overall severity of IBD histopathology, particularly with active inflammation. Th17 is also associated with activity. By contrast, IL-22+ cells are associated with chronicity and granuloma formation in CD.
炎症性肠病(IBD)主要是由于 CD4+辅助性和调节性 T 细胞的异常而引起的,其组织病理学表现为慢性活动性结肠炎,具有反映黏膜炎症活动和慢性的特征。IBD 的确切免疫组织学相关性尚不清楚。
我们研究了溃疡性结肠炎(UC)和克罗恩病(CD)结肠黏膜 CD4+T 细胞亚群(Th1、Th2、Th17、Th22 和 Treg)与黏膜组织学变化之间的相关性。通过流式细胞术进行 CD4+T 细胞亚群分型和计数。使用三种经过验证的组织学评分方案(ECAP、RHI 和 D'Haens)对组织学特征进行分类和半定量评估。分析 CD4+T 细胞亚群的流行率(%)与组织学评分之间的相关性。
Treg 细胞与 ECAP 类别 A(活动期)以及 RHI 评分相关。Treg 细胞在黏膜中严重中性粒细胞浸润、隐窝/表面上皮和固有层以及基底浆细胞增多时增加。在固有层广泛中性粒细胞浸润的病例中,Th17 细胞也增加,而在固有层严重淋巴浆细胞浸润的病例中,RORc+细胞增加。在 UC 和 CD 中,具有明显隐窝结构改变的黏膜中,IL-22+和 Th22 细胞增加。具有潘氏细胞化生的 UC 中 Th17 细胞增加。具有肉芽肿的 CD 中,IL-22+和 IL-22+IFN-γ+细胞增加。
Treg 亚群似乎与 IBD 组织病理学的总体严重程度相关,特别是与活动性炎症相关。Th17 也与活性相关。相比之下,IL-22+细胞与 CD 中的慢性和肉芽肿形成相关。