Th17细胞是首个被确定有别于Th1/Th2模式的亚群，且基于IL-23刺激后IL-17A同型二聚体的表达。 Th17细胞生成另一个同型二聚体IL-17家族成员IL-17F，以及异质二聚体蛋白IL-17AF，IL-17AF由IL-17A的一个亚基和IL-17F的一个亚基组成。 IL-17介导的反应在上皮细胞、内皮细胞和成纤维细胞中最具特征，这些细胞通过分泌TNFα、IL-1β、IL-6、IL-8、CXCL1、CXCL8和G-CSF来应答IL-17R信号，从而促进中性粒细胞募集和炎症反应。 细胞因子IL-22是IL-10家族成员之一，研究 …

Recently T-helper 17 (Th17) cells were demonstrated to disrupt the blood-brain barrier (BBB) by the action of IL-17A. The aim of the present study was to examine the mechanisms that underlie IL-17A-induced BBB breakdown. Barrier integrity was analyzed in …

IL-17驱动的炎症通常由调节性T细胞和抗炎细胞因子 IL-10 、 TGF-β 和 IL-35 调控。 然而，如果失调，IL-17反应可促进感染或自身免疫的免疫病理学。 此外，IL-17还参与了许多其他炎症性疾病的发病机制，包括心血管和神经系统疾病。 因此，IL-17途径现在是许多自身免疫性和慢性炎症性疾病的关键药物靶点。 Th17细胞在体内的细胞因子产生中显示出一定的可塑性，可以从主要产生IL-17转变为主要产生 IFN-γ，从而类似于TH1细胞。 Th17细胞的可塑性受T细胞极化细胞因子和 …

2023年2月6日 · th17细胞可表达高水平的il-23受体和颗粒酶b，以使其能够通过血脑屏障（bbb）迁移并随后促成慢性cns炎症。 Th17细胞的大量浸润导致Th17细胞与免疫抑制Treg之间的失衡，这与该自身免疫性疾病的发生和发展密切相关。

Infusion of FITC-linked albumin in blood circulation and combination with immunostaining of hippocampal sections for RORγ, a specific transcriptional factor of Th17 cells, demonstrated blood-brain barrier (BBB) disruption and Th17 cells’ infiltration into brain parenchyma of AD rats.

Once in the brain parenchyma, Th17 cells release several proinflammatory mediators including IL-17A, responsible for the downregulation of tight junction proteins of the BBB, increasing BBB permeability, and favoring migration of both soluble inflammatory molecules and other circulating immune cells into the CNS .

辅助性T 细胞17 (T helper cell 17, Th17)是一种新发现的能够分泌白介素17 (interleukin 17, IL-17)的T 细胞亚群，在自身免疫性疾病和机体防御反应中具有重要的意义。 β 转化生长因子 (transforming growth factor b, TGF-β)、IL-6、IL-23 和IL-21 在Th17 细胞的分化形成过程中起着积极的促进作用，而γ 干扰素 (interferon γ, IFN-γ)、IL-4、细胞因子信号传送阻抑蛋白3 (suppressor of cytokine signaling 3, Socs3)和IL-2则抑制它的分化。 [1]

In recent reviews, the Th17 cell lineage has been described as the third major subset of effector T cells, as these cells help regulate neutrophils while Th2 cells regulate eosinophils and Th1 cells regulate macrophages. Thus, the three groups dynamically alter myeloid cells 3.

2020年8月21日，清华大学免疫学研究所董晨院士团队在Cell Press细胞出版社期刊Immunity上发表题为“The conserved non-coding sequences CNS6 and CNS9 control cytokine-induced Rorc transcription during T helper 17 cell differentiation”的文章，发现起始Th17细胞分化所必需的两个细胞因子IL-6和TGF-β，通过与Rorc基因位点两个不同的保守非编码DNA序列（conserved non-coding sequence, CNS）相互作用，协同调控RORγt的表达及Th17细胞分化。

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