Rheumatoid arthritis (RA) is a chronic, systemic, and autoimmune disease, and its main pathological changes are inflammatory cell infiltration accompanied by the secretion and accumulation of a variety of related cytokines, which induce the destruction of cartilage and bone tissue. Therefore, the modulation of inflammatory cells and cytokines is a key therapeutic target for controlling inflammation in RA. This review details the effects of emodin on the differentiation and maturation of T lymphocytes, dendritic cells, and regulatory T cells. In addition, the systematic introduction of emodin directly or indirectly affects proinflammatory cytokines (TNF-α, IL-6, IL-1, IL-1β, IL-17, IL-19, and M-CSF) and anti-inflammatory cytokines (the secretion of IL-4, IL-10, IL-13, and TGF-β) through the coregulation of a variety of inflammatory cytokines to inhibit inflammation in RA and promote recovery. Understanding the potential mechanism of emodin in the treatment of RA in detail provides a systematic theoretical basis for the clinical application of emodin in the future.