Abstract
Objective To investigate the relationship between serum interleukin-2 (IL-2) levels and disease activity, absolute numbers of peripheral lymphocyte subsets, autoantibodies, and associated cytokines in patients with rheumatoid arthritis (RA). Methods This study included 106 patients with RA, evaluated their disease activity (DAS28 score), and divided them into disease remission (DAS28 ≤ 2.6), low disease activity (DAS28 ≤ 3.2), and moderate-high disease activity (DAS28 > 3.2) groups. Flow cytometry was used to detect the absolute numbers of peripheral lymphocyte subpopulations and CD4+ T cell subsets in each group, and serum cytokine levels were measured using cytometric bead array. Results Serum IL-2 levels in RA patients were positively correlated with disease activity and rheumatoid factor titers (p < 0.001 and p = 0.045, respectively), and multiple regression analysis revealed that serum IL-2 levels were an independent factor affecting disease activity. Serum IL-2 levels were positively correlated with Th17/Treg ratios (p = 0.013). Compared with the remission group, peripheral lymphocyte and CD4+ T lymphocyte subsets in patients with active RA decreased to varying degrees; however, the numbers of peripheral natural killer (NK) cells were significantly higher in the moderate-high disease activity group than in the remission (p = 0.046) and low disease activity (p = 0.020) groups; the percentages of NK cells had the same trend. In addition, the number and percentage of NK cells were positively correlated with serum IL-2 levels (p = 0.018 and p = 0.006, respectively). Conclusions In RA patients, serum IL-2 levels were not only correlated with patients' disease activity and autoantibody levels but were also involved in their Th17/Treg immune imbalance. In addition, in patients with active RA, NK cell levels were abnormally elevated, possibly due to high serum levels of IL-2.
Highlights
Rheumatoid arthritis (RA) is a systemic, inflammatory, autoimmune disease that causes progressive joint damage that can lead to lifelong disability
Recent studies have shown that interleukin 2 (IL-2) is a key cytokine that affects the differentiation of immune cells and has pleiotropic effects: it activates effector T cells to promote immune response and promotes Treg cell proliferation to maintain immune tolerance, playing important roles in infection, autoimmune diseases, and cancer
In patients with RA, whether serum IL-2 levels are related to disease activity, whether they affect the development and differentiation of lymphocyte subsets and the potential therapeutic prospect of low-dose IL-2 in RA are clinical frontier hotspots
Summary
Rheumatoid arthritis (RA) is a systemic, inflammatory, autoimmune disease that causes progressive joint damage that can lead to lifelong disability. This systemic disease is characterized by synovial inflammatory cell infiltration, synovial hyperplasia, angiogenesis, cartilage, and bone erosion [1]. T cells and other infiltrating immune cells associated with the disease release a variety of cytokines, which are important mediators of cell differentiation, inflammation, immune pathology, and immune response [2]. Recent studies have demonstrated the pleiotropy of IL-2: it both activates traditional T cells to promote the immune response and promotes regulatory T (Treg) cell proliferation to control the inflammatory response and maintain immune tolerance as a cytokine necessary for Treg cell development and Mediators of Inflammation homeostasis [6, 7]. In RA patients, the relationships among serum IL-2 levels and disease activity, Th17/Treg immune balance, peripheral blood lymphocyte subpopulation counts, RA-specific autoantibodies such as rheumatoid factor (RF) and anticyclic citrullinated peptide (CCP), and serum levels of other cytokines have rarely been reported
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