The immune-pathology in Crohn’s disease is linked to dysregulated CD4+ T cell responses biased towards pathogenic TH17 cells. However, the role of CD8+ T cells able to produce IL-17 (Tc17 cells) remains unclear. Here we characterize the peripheral blood and intestinal tissue of Crohn’s disease patients (n = 61) with flow and mass cytometry and reveal a strong increase of Tc17 cells in active disease, mainly due to induction of conventional T cells. Mass cytometry shows that Tc17 cells express a distinct immune signature (CD6^high, CD39, CD69, PD-1, CD27^low) which was validated in an independent patient cohort. This signature stratifies patients into groups with distinct flare-free survival associated with differential CD6 expression. Targeting of CD6 in vitro reduces IL-17, IFN-γ and TNF production. These results identify a distinct Tc17 cell population in Crohn’s disease with proinflammatory features linked to disease activity. The Tc17 signature informs clinical outcomes and may guide personalized treatment decisions.

克罗恩病的免疫病理学与偏向致病性 TH17 细胞的失调的 CD4+ T 细胞反应有关。然而，能够产生 IL-17（Tc17 细胞）的 CD8+ T 细胞的作用仍不清楚。在这里，我们用流式细胞术和大规模细胞术对克罗恩病患者 (n = 61) 的外周血和肠组织进行了表征，并揭示了活动性疾病中 Tc17 细胞的强烈增加，这主要是由于常规 T 细胞的诱导。质谱流式细胞术显示 Tc17 细胞表达独特的免疫特征（CD6^高、CD39、CD69、PD-1、CD27^低) 在独立的患者队列中得到验证。该特征将患者分层为具有与差异 CD6 表达相关的明显无耀斑存活率的组。体外靶向 CD6 可减少 IL-17、IFN-γ 和 TNF 的产生。这些结果确定了克罗恩病中具有与疾病活动相关的促炎特征的独特 Tc17 细胞群。Tc17 签名告知临床结果，并可能指导个性化治疗决策。