SLE is an autoimmune inflammatory disease in which various pro- and anti-inflammatory cytokines, including TGF-β, IL-10, BAFF, IL-6, IFN-α, IFN-γ, IL-17, and IL-23, play crucial pathogenic roles. Virtually, all these cytokines can be generated by both innate and adaptive immune cells and exert different effects depending on specific local microenvironment. They can also interact with each other, forming a complex network to maintain delicate immune homeostasis. In this paper, we elaborate on the abnormal secretion and functions of these cytokines in SLE, analyze their potential pathogenic roles, and probe into the possibility of them being utilized as targets for therapy.

γ δ T cells are a minor population of T cells that express the TCR γ δ chains, mainly distributed in the mucosal and epithelial tissue and accounting for less than 5% of the total T cells in the peripheral blood. By bridging innate and adaptive immunity, γ δ T cells play important roles in the anti-infection, antitumor, and autoimmune responses. Previous research on γ δ T cells was primarily concentrated on infectious diseases and tumors, whereas their functions in autoimmune diseases attracted much attention. In this paper, we summarized the various functions of γ δ T cells in two prototypical autoimmune connective tissue diseases, that is, SLE and RA, elaborating on their antigen-presenting capacity, secretion of proinflammatory cytokines, immunomodulatory effects, and auxiliary function for B cells, which contribute to overproduction of proinflammatory cytokines and pathogenic autoantibodies, ultimately leading to the onset of these autoimmune diseases. Elucidation of the roles of γ δ T cells in autoimmune diseases is not only conducive to in-depth understanding of the pathogenesis of these diseases, but also beneficial in providing theoretical support for the development of γ δ T-cell-targeted therapy.

Aim: cd T cells exhibit important functions in the pathogenesis of rheumatoid arthritis (RA). In recent years, numerous studies harnessed the cd T cell-activating capacity of aminobiphosphonates for the treatment of malignant tumors. As

ObjectiveTo investigate the association of serum with disease activity and occurrence of interstitial lung disease (ILD) in patients with rheumatoid arthritis (RA). MethodsOne hundred and six RA patients were included, including 31 with ILD. All patients were divided into two groups according to the 28-joint Disease Activity Score (DAS28), active-disease group (DAS28>3.2) and target-achieved group (DAS28≤3.2). Serum IL-11 was detected by ELISA. Serum autoantibodies [anticitrullinated protein antibody (ACPA) and rheumatoid factor (RF)], inflammatory markers [C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)], and complete blood count were measured with routine methods. Results Serum IL-11 was upregulated in RA patients compared with healthy controls (HC), and increased more significantly in patients with ILD (RA-ILD) than patients without ILD (RA-nonILD). In both RA-ILD and RA-nonILD patients, serum level of IL-11 was higher in the active-disease group than that in the target-achieved group. Pearson correlation analysis confirmed that IL-11 was positively correlated with DAS28. No significant correlation was found between serum level of IL-11 and ACPA or RF. IL-11 was positively correlated with ESR and CRP levels and PLT count in RA patients. Conclusion IL-11 was found to be involved in the development of arthritis and ILD in RA patients, and might constitute a potential target for the treatment of RA-ILD.

To retrospectively analyze the efficacy and safety of febuxostat on gout patients with low serum uric acid level. A study was conducted in Nanjing First Hospital from October 2015 to September 2016. Thirty nine acute gouty arthritis patients from the emergency and outpatient department were included. Patients met the 2015 Gout Classification Criteria revised by American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) and had urate deposition around the joints detected by dual-energy computerized tomography (DECT). Patients whose serum uric acid (SUA) were between 5.0 and 7.0 mg/dl (300-420 μmol/l) received febuxostat treatment to maintain the SUA level between 3.0 and 5.0 mg/dl for 1 year. Efficacy and safety of febuxostat were observed during the process. Three of 39 subjects were excluded because of adverse events (AEs) after receiving an initial febuxostat treatment for 2 months. Thirty six subjects were enrolled. The mean SUA level was reduced significantly from 6.51 ± 0.28 mg/dl at baseline to 4.24 ± 0.38 mg/dl and SUA of all subjects decreased by 34.8% compared with baseline. After 1-year treatment, the volume of tophus was reduced approximately 62.8%. Serum creatinine decreased stepwise in 8 gout patients with chronic kidney diseases from 162.5 ± 9.2 μmol/l to 131.4 ± 11.0 μmol/l. Two months after initiation of treatment, the number of gout flares began to markedly decrease and almost did not occur after 1 year. After the 1-year treatment of febuxostat, the average SUA level declined significantly, and the renal function improved gradually. There was nearly complete abolition of gout flares by the end of the study. Tophi resolved markedly compared with baseline as assessed by DECT. Furthermore, only a few people experienced adverse events. Febuxostat has a notable effect for gout patients in the lower SUA level range.