At mucosal barriers, the T helper 17 (T_H17) cell population plays a fundamental role in controlling tissue homeostasis. The adaptability of this population to a more pro-inflammatory or anti-inflammatory function — that is, their functional plasticity and consequently heterogeneity — primarily depends on the environment. We would like to term this process environmental immune adaptation. Interfering with T_H17 cell adaptation leads to pathological consequences, including development of immune-mediated inflammatory diseases or even cancer. Several molecular mechanisms have been shown to participate in this process and recently, a better understanding of the transcriptional and metabolic profiling of T_H17 cells has shed light on a new level of complexity. Here, we offer a summary on the role of T_H17 cell plasticity in inflammatory diseases and cancer as well as the latest discoveries and controversies regarding the mechanisms that control the adaptability of the T_H17 cell population.

在粘膜屏障处，辅助 T 17 (TH ₁₇ ) 细胞群在控制组织稳态中发挥着重要作用。该群体对促炎或抗炎功能的适应性（即功能可塑性和由此产生的异质性）主要取决于环境。我们想将此过程称为环境免疫适应。干扰 T _H 17 细胞适应会导致病理后果，包括免疫介导的炎症性疾病甚至癌症的发展。多种分子机制已被证明参与这一过程，最近，对 T _H 17 细胞转录和代谢谱的更好理解使复杂性达到了新的水平。在此，我们总结了 T _H 17 细胞可塑性在炎症性疾病和癌症中的作用，以及有关控制 T _H 17 细胞群适应性机制的最新发现和争议。