The Chemokine Biology Laboratory, Department of Molecular and Biomedical Science, School of Biological Sciences, Faculty of Science, The University of Adelaide, Adelaide, SA, Australia.
Front Immunol. 2022 Feb 16;13:817473. doi: 10.3389/fimmu.2022.817473. eCollection 2022.
Pro-inflammatory CD4 T helper (Th) cells drive the pathogenesis of many autoimmune conditions. Recent advances have modified views of the phenotype of pro-inflammatory Th cells in autoimmunity, extending the breadth of known Th cell subsets that operate as drivers of these responses. Heterogeneity and plasticity within Th1 and Th17 cells, and the discovery of subsets of Th cells dedicated to production of other pro-inflammatory cytokines such as GM-CSF have led to these advances. Here, we review recent progress in this area and focus specifically upon evidence for chemokine receptors that drive recruitment of these various pro-inflammatory Th cell subsets to sites of autoimmune inflammation in the CNS. We discuss expression of specific chemokine receptors by subsets of pro-inflammatory Th cells and highlight which receptors may be tractable targets of therapeutic interventions to limit pathogenic Th cell recruitment in autoimmunity.
促炎 CD4 T 辅助(Th)细胞驱动许多自身免疫性疾病的发病机制。最近的进展改变了人们对自身免疫中促炎 Th 细胞表型的看法,扩展了已知作为这些反应驱动因素的 Th 细胞亚群的范围。Th1 和 Th17 细胞的异质性和可塑性,以及发现专门产生其他促炎细胞因子(如 GM-CSF)的 Th 细胞亚群,导致了这些进展。在这里,我们回顾该领域的最新进展,并特别关注趋化因子受体的证据,这些趋化因子受体驱动各种促炎 Th 细胞亚群招募到中枢神经系统自身免疫炎症部位。我们讨论了促炎 Th 细胞亚群中特定趋化因子受体的表达,并强调了哪些受体可能是治疗干预的可行靶点,以限制自身免疫中的致病性 Th 细胞募集。