Mechanisms regulating the loss of Tregs in HUPO mice that develop spontaneous inflammatory arthritis

The efficacy and safety of short-term and low-dose IL-2 combined with tocilizumab to treat rheumatoid arthritis

“…According to the production of cytokines and the expression of main transcription factors, CD4+T cells are roughly divided into CD4+T helper (Th) cells such as Th1, Th2, and Th17 cells, which can regulate the inflammatory environment, promote antibody production, control innate immunity and stimulate immune memory, and anti-inflammatory CD4+T groups, namely Treg, which inhibit inflammation, dominant self-tolerance, maintain immune homeostasis and control immune responses to prevent autoimmune diseases ( 34 ). Inflammation is usually accompanied by dysregulation of CD4+T cell subsets and cytokine networks, which play a dominant role in immune regulation, characterized by excessive proliferation of inflammatory cells or depletion or dysfunction of regulatory cells, and ultimately the inflammation gets aggravated ( 19 , 21 ). As observed in this study, the absolute count of peripheral Tregs and the ratio of Th17 to Treg were strongly associated with the disease activities of RA.…”

“…Evidence from numerous studies indicates that the imbalance of CD4+T cell subsets, especially the significant reduction in T regulatory cells (Tregs) responsible for maintaining immune homeostasis and suppressing inflammatory response, contributes to joint damage and disease deterioration in RA ( 19 ). Tregs have emerged as potential therapeutic targets for many autoimmune diseases such as RA ( 20 , 21 ). Initial data indicate that the number of circulating Tregs in RA patients decreases with increasing disease activity, which can be reversed by exogenous supplementation with low doses of IL-2 ( 22 ).…”

The differentiation courses of the Tfh cells: a new perspective on autoimmune disease pathogenesis and treatment

“…The occurrence and development of AID also involve other cells, including Treg cells. Treg cells are essential for immunosuppressive, maintenance self-tolerance and suppressing autoimmunity through the production of anti-inflammatory cytokines, and a deficiency of Treg cells results in fatal AID in humans and mice [ 122 ]. Increased plasticity of Tfh cells and CD4 + T cells polyfunctionality with enriched memory Treg cell responses was demonstrated in RA patient synovial tissue, identified the presence of a novel population of pathogenic polyfunctional T cells that are enriched in the RA joint [ 123 ].…”