趋化因子在通过白细胞从血液循环进入炎症关节中引发并持续滑膜炎过程中扮演关键角色。大量文献研究了双重功能干扰素（IFN）致敏趋化因子CXCL9、CXCL10和CXCL11在慢性炎症性关节病中的作用，强调有必要澄清它们的发病病理关联。通过与彼此共同的受体CXC趋化因子受体3（CXCR3）相互作用，CXCL9、CXCL10和CXCL11趋化因子发挥了它们协调CD4+TH1细胞、CD8+T细胞、NK细胞和NKT细胞朝向炎症风险区的方向性移动的特点功能。IFN诱导CXCR3配体被认为与自身炎症和自身免疫性疾病有关，此外还涉及感染、癌症和血管生成等其他病理生理过程。本文综述了IFN诱导CXCR3配体在炎症性关节炎患者体液中的大量存在，它们在啮齿动物模型中的选择性清除结果，以及试图开发靶向CXCR3趋化因子系统的候选药物的进展。我们进一步提出，CXCR3结合趋化因子在滑膜炎和关节重塑中的作用远远不止于CXCR3表达白细胞的方向性进入。在滑膜微环境中IFN诱导CXCR3配体的多效作用反复说明了CXCR3趋化因子网络的极其复杂性，其基础是IFN诱导的CXCR3配体与存在于炎症关节中的不同CXCR3亚型、酶、细胞因子和浸润和定居细胞的交流互通。©2023。作者使用授权独家许可给Springer Nature Switzerland AG。

Chemokines are pivotal players in instigation and perpetuation of synovitis through leukocytes egress from the blood circulation into the inflamed articulation. Multitudinous literature addressing the involvement of the dual-function interferon (IFN)-inducible chemokines CXCL9, CXCL10 and CXCL11 in diseases characterized by chronic inflammatory arthritis emphasizes the need for detangling their etiopathological relevance. Through interaction with their mutual receptor CXC chemokine receptor 3 (CXCR3), the chemokines CXCL9, CXCL10 and CXCL11 exert their hallmark function of coordinating directional trafficking of CD4+ TH1 cells, CD8+ T cells, NK cells and NKT cells towards inflammatory niches. Among other (patho)physiological processes including infection, cancer, and angiostasis, IFN-inducible CXCR3 ligands have been implicated in autoinflammatory and autoimmune diseases. This review presents a comprehensive overview of the abundant presence of IFN-induced CXCR3 ligands in bodily fluids of patients with inflammatory arthritis, the outcomes of their selective depletion in rodent models, and the attempts at developing candidate drugs targeting the CXCR3 chemokine system. We further propose that the involvement of the CXCR3 binding chemokines in synovitis and joint remodeling encompasses more than solely the directional ingress of CXCR3-expressing leukocytes. The pleotropic actions of the IFN-inducible CXCR3 ligands in the synovial niche reiteratively illustrate the extensive complexity of the CXCR3 chemokine network, which is based on the intercommunion of IFN-inducible CXCR3 ligands with distinct CXCR3 isoforms, enzymes, cytokines, and infiltrated and resident cells present in the inflamed joints.© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.