Department of Medicine, Division of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts; Translational Research Program, Benroya Research Institute, Seattle, Washington; Division of Internal Medicine, University of Washington, Seattle, Washington.
Translational Research Program, Benroya Research Institute, Seattle, Washington.
Cell Mol Gastroenterol Hepatol. 2020;10(3):507-526. doi: 10.1016/j.jcmgh.2020.04.013. Epub 2020 May 1.
BACKGROUND & AIMS: Crohn's disease (CD) likely represents decreased immune tolerance to intestinal bacterial antigens. Most CD patients have high titers of antibodies to intestinal commensal proteins, including the outer membrane porin C (OmpC) of Escherichia coli.
By using major histocompatibility complex II tetramers, we identified an HLA-DRB1∗15:01-restricted peptide epitope of OmpC recognized by CD4+ T cells in peripheral blood mononuclear cells from HLA-DRB1∗15:01+ healthy control (HC) and CD patients.
The precursor frequency of these cells in CD correlated with anti-OmpC IgA titers, but did not differ from that of HCs. In both cohorts, they showed a CD161+, integrin α4β7+ phenotype ex vivo by flow cytometry, distinct from the C-X-C Motif Chemokine Receptor 3 phenotype of autologous influenza hemagglutinin (Flu) peptide-specific T cells. The T-cell receptor α and β chains of in vitro-expanded OmpC-specific T-cell clones often contained public amino acid sequences that were identical in cells from different patients. Expanded T-cell clones from CD subjects produced significantly less interleukin (IL)10 (P < .0001) than those from HCs, and a trend toward decreased production of the T helper 2 cell-associated IL4, IL5, and IL13 by CD clones also was seen.
Both HCs and CD patients have detectable OmpC-specific T cells in circulation, with similar immunophenotypes and often identical T-cell-receptor sequences. However, expanded clones from patients with CD produce less of the immunoregulatory cytokine IL10, showing a selective defect in the regulatory function of intestinal microbial antigen-specific T cells in patients with CD.
克罗恩病(CD)可能代表对肠道细菌抗原的免疫耐受降低。大多数 CD 患者对肠道共生蛋白,包括大肠杆菌的外膜孔蛋白 C(OmpC),具有高滴度的抗体。
通过使用主要组织相容性复合物 II 四聚体,我们鉴定了 CD4+T 细胞在 HLA-DRB1∗15:01+健康对照(HC)和 CD 患者外周血单核细胞中识别的 OmpC 的 HLA-DRB1∗15:01 限制性肽表位。
这些细胞在 CD 中的前体频率与抗-OmpC IgA 滴度相关,但与 HC 没有差异。在两个队列中,它们通过流式细胞术显示出 CD161+、整合素α4β7+表型,与自体流感血凝素(Flu)肽特异性 T 细胞的 C-X-C 基序趋化因子受体 3 表型不同。体外扩增的 OmpC 特异性 T 细胞克隆的 T 细胞受体α和β链通常包含来自不同患者的细胞中相同的公共氨基酸序列。来自 CD 受试者的扩增 T 细胞克隆产生的白细胞介素(IL)10 明显少于 HC(P <.0001),并且还观察到 CD 克隆产生的辅助性 T 细胞 2 相关 IL4、IL5 和 IL13 的产生趋势降低。
HC 和 CD 患者的循环中都存在可检测的 OmpC 特异性 T 细胞,具有相似的免疫表型,并且经常具有相同的 T 细胞受体序列。然而,来自 CD 患者的扩增克隆产生的免疫调节细胞因子 IL10 较少,表明 CD 患者肠道微生物抗原特异性 T 细胞的调节功能存在选择性缺陷。