Rheumatoid arthritis (RA) is an autoimmune disorder that affects joints associated with inflammation leading to poor quality of life. The phenotype of RA is distinct from osteoarthritis (OA), the degenerative joint disorder. The annual incidence of RA is approximately 4 in 10,000 individuals. Studies suggest dysregulated T cell activation in the initiation and progression of RA. Distinct RA-associated allelic variants encode molecules involved in T-cell activation pathways. Additionally, RA is also associated with aberrant regulation and function of T helper cells. The interplay of distinct T helper cell subsets adds complexity to the regulation of RA. In this review we have aimed to understand the currently known biology of different Th subsets in the context of an autoimmune disease like rheumatoid arthritis and find potential therapeutic approaches to tackle the disease through modulation of responsible T cells.

类风湿关节炎（RA）是一种自身免疫性疾病，会影响与炎症相关的关节，导致生活质量下降。RA的表型不同于变性关节炎（OA）。RA的年发病率约为10,000个人中的4个人。研究表明在RA的发生和发展过程中T细胞活化失调。与RA相关的不同等位基因变体编码参与T细胞活化途径的分子。另外，RA还与T辅助细胞的异常调节和功能有关。不同的T辅助细胞亚群的相互作用增加了RA调控的复杂性。