Rheumatoid arthritis (RA) is an autoimmune disease that involves T and B cells and their reciprocal immune interactions with proinflammatory cytokines. T cells, an essential part of the immune system, play an important role in RA. T helper 1 (Th1) cells induce interferon-?? (IFN-??), tumour necrosis factor-?? (TNF-??), and interleukin (IL)- 2, which are proinflammatory cytokines, leading to cartilage destruction and bone erosion. Th2 cells primarily secrete IL- 4, IL- 5, and IL- 13, which exert anti- inflammatory and anti- osteoclastogenic effects in inflammatory arthritis models. IL- 22 secreted by Th17 cells promotes the proliferation of synovial fibroblasts through induction of the chemokine C- C chemokine ligand 2 (CCL2). T follicular helper (Tfh) cells produce IL- 21, which is key for B cell stimulation by the C- X- C chemokine receptor 5 (CXCR5) and coexpression with programmed cell death- 1 (PD- 1) and/or inducible T cell costimulator (ICOS). PD- 1 inhibits T cell proliferation and cytokine production. In addition, there are many immunomodulatory agents that promote or inhibit the immunomodulatory role of T helper cells in RA to alleviate disease progression. These findings help to elucidate the aetiology and treatment of RA and point us toward the next steps.