BackgroundRelapsing polychondritis (RP) is an rare inflammatory disease of unknown causes, characterized by recurrent inflammation in cartilaginous tissues of the whole body[1]. The histologic features of the chondritis include loss of basophilic staining of the cartilage matrix, perichondrial inflammation, cartilage destruction with replacement by fibrous tissue, and perivascular cellular infiltration with plasma cells and lymphocytes. Additional clinical features of the disease include ocular inflammation, vasculitis, audiovestibular dysfunction, myocarditis, cardiac valvular insufficiency, and nonerosive inflammatory arthritis. Many studies have shown that the imbalance of helper T cell 17(Th17) and regulatory T cell(Treg) is involved in the pathogenesis of autoimmune diseases such as SLE and RA. But little is known about the roles of peripheral immune cell subsets peripheral in RP patients. Up to now, just few studies focus on this issue.ObjectivesWe aimed to analyse the distribution and phenotype of CD4+T cell subsets in the peripheral blood of patients with RP.MethodsThe proportion and absolute counts of circulating immune cells were assessed in 14 patients diagnosed as RP and 14 healthy controls. CD4+T cell subsets were also analysed in 9 untreated RP patients and 9 healthy volunteers by flow cytometry. All statistical analyses were performed with SPSS v. 22.0. Continuous variables were reported as median. For all study variables, comparison among controls and RP subjects was based on the non-parametric Wilcoxon Mann-Whitney exact test. For all analyses, we used two-sided tests, with p-values <0.05 denoting statistical significance.ResultsProportion and absolute counts of Treg cells were significantly reduced in RP patients in comparison with controls (proportion, 3.61% vs. 5.24%, p<0.001; absolute counts, 27.36/μl vs. 46.56/μl,p<0.001). But there were no significant difference between the percentage and number of Th17, Th1 or Th2 cells in patients with RP and healthy controls. Thus, the ratio of Th17/Treg increased in RP patients (0.25 vs. 0.14, p<0.001), as did the ratio of Th2/Treg (0.28 vs. 0.22, p<0.001) and Th1/Treg(2.75 vs. 1.92, p=0.019)(Figue 1). Similarly, the proportion and absolute counts of Treg cells in untreated RP patients were significantly lower than that in healthy controls (proportion, 3.78% vs. 5.66%, p=0.008; absolute counts, 32.24/μl vs. 50.76/μl, p<0.001).And the ratio of Th17/Treg slso increased in untreated RP patients (0.25 vs. 0.15, p=0.003), as did the ratio of Th1/Treg (2.35 vs. 1.88, p=0.014)(Figue 2).ConclusionOur data suggested that the immune-inflammation in RP patients may be related to the depletion of Treg cells and the imbalance of Th17 or Th1 or Th2 and Treg cells.Reduction of peripheral Treg cells may exacerbate the disease progression by not being inhibited Th cells.Reference[1] Kingdon J, Roscamp J, Sangle S, et al. Relapsing polychondritis: a clinical review for rheumatologists[J]. Rheumatology, 2017, 57(9): 1525-1532.AcknowledgementRheumatology and laboratory staf...

To evaluate the preventive effect and enhance immunity functions of Bu-zhong-yi-qi wan in vivo. Materials and Methods: S180 tumor mice model was established by subcutaneous injection a dose of 0.2 ml (1×10 7 /ml) at the right oxter. The inhibitory rates, spleen indexes and thymus indexes were calculated. Splenic lymphocyte proliferative activity assay and phagocytosis activity of peritoneal macrophages were done. Interferon (IFN-γ), interleukin (IL-2) and tumor necrotic factor (TNF-α) in serum were detected. Results: In the S180 tumor-bearing mice, Bu-zhong-yi-qi wan with medium-dose (975 mg/kg, 100 mg/l) had potent preventive effect and anti-tumor effect, macrophage phagocytosis and Con A-stimulated splenocyte proliferation were increased as compared with model control treatment. Bu-zhong-yi-qi wan could take part in the immune response by promoting the proliferation and differentiation of Tcells, increasing the activity of the macrophages, inducing the generation of cell factor IL-2, TNF-α, IFN-γ. Conclusion: It proved that Bu-zhong-yi-qi wan of medium-dose had great preventive effect and could enhance immunity function.

BackgroundWe have reported previously that the insufficient absolute number or functional defects of regulatory T cells (Tregs) in patients with rheumatoid arthritis (RA)[ 1-3 ], challenging conventional unspecific immunosuppressive therapy. Sirolimus, a mTOR inhibitor, is reported to allow growth of functional Tregs, which would be able to provide new strategy and target for the treatment of RA[ 4 ].ObjectivesTo investigate efficacy and safety of sirolimus combined with conventional immunosuppressants for RA treatment.MethodsIn this non-blinded and parallel-group trial, we randomly assigned 62 patients to receive conventional glucocorticoids and immunosuppressants with or without sirolimus at a dosage of 0.5 mg on alternate days for 24 weeks in a 2:1 ratio. The demographic features, clinical manifestations and laboratory indicators including peripheral blood lymphocyte subgroups and CD4+T subsets were compared before and after the treatment.ResultsFinally, 37 patients in sirolimus group and 18 in conventional treated group completed 6-month study. By 24 weeks, the patients with sirolimus experienced the significant reduction in disease activity indicators including DAS28, ESR, the number of tender joints and swollen joints (p<0.001). Notably, they had a higher level of Tregs as compared those with conventional therapy alone (p<0.05), indicating that sirolimus could partly restore the reduced Tregs. Concomitantly, their usages of immunosuppressants for controlling disease activity were decreased as compared with conventional group with no difference in blood routine, liver and renal functions both before and after the treatment of sirolimus and between two groups (p>0.05).ConclusionLow-dose sirolimus immunoregulatory therapy selectively up-regulated Tregs and partly replaced the usage of immunosuppressants to control disease activity without over-treatment and evaluable side effect. The further study is required using a large sample of RA patients treated with sirolimus for longer period.References[1] Komatsu N, Takayanagi H. Arthritogenic T cells in autoimmune arthritis[J]. The international journal of biochemistry & cell biology, 2015, 58:92-96.doi:10.1016/j.biocel.2014.11.008.[2] Morita T, Shima Y, Wing JB, et al. The Proportion of Regulatory T Cells in Patients with Rheumatoid Arthritis: A Meta-Analysis[J]. PloS one, 2016, 11(9):e0162306.doi:10.1371/journal.pone.0162306.[3] Spence A, Klementowicz JE, Bluestone JA, et al. Targeting Treg signaling for the treatment of autoimmune diseases[J]. Current opinion in immunology, 2015, 37:11-20.doi:10.1016/j.coi.2015.09.002.[4] Perl A. Activation of mTOR (mechanistic target of rapamycin) in rheumatic diseases[J]. Nature reviews Rheumatology, 2016, 12(3):169-182.doi:10.1038/nrrheum.2015.172.AcknowledgementNoDisclosure of InterestsNone declared

(MIC: 1.6 mg/mL, MBC: 3.2 mg/mL). Besides, Sanqixiantao extracts (100, 200, p < 0.01, p < 0.01, p < 0.01

BackgroundRheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by synovitis and vasospasm[1]. So far, The biggest challenge in the current field of RA treatment is the production of DMARDs multidrug resistance (MDR) and the most critical mechanism for the production of MDR is the ABC transporter family-mediated increase in target cell drug excretion, while inflammatory cytokines play an important role in its expression regulation. Our previous research have confirmed that IL-1β, IL-6 and IL-17 are involved in the regulation of P-glycoprotein (P-gp) expression in lymphocytes of RA patients. The breast cancer resistance protein (BCRP/ABCG2) is also a highly efficient efflux pump, which absorbs, distributes, and excretes drugs or exogenous substances in the body[2]. IL-1βis a cytokine involved in the whole process of RA, which can aggravate the inflammatory response. However, there is no research on the effect of IL-1β on the expression of BCRP in RA Fibroblast-like synoviocytes (FLS).ObjectivesTo explore the effects of different concentrations of IL-1β on the expression of drug resistance proteins in FLS of RA patients at different time points.MethodsSynovial tissues of untreated RA patients (n=3) were extracted by Joint surgery, FLS culture system in vitro was established and passaged to the fifth generation or so to do the experiments. FLS cells were divided into A, B, C, D four groups randomly with different treatments: Group A was the cell control group. Group B, C, D were respectively co-cultured with low (20ng/ml), middle (50ng/ml), high (100ng/ml) concentrations of IL-1β. They were cultured respectively for 24 hours, 48 hours, and 72 hours. The effect of IL-1β on the expression level of BCRP mRNA was observed at different concentrations and at different time points.ResultsWith the prolongation of IL-1βculture, the expression of BCRP mRNA increased. Under the same concentration of IL-1β(20ng/ml or 50ng/ml), the expression of BCRP mRNA in the 72h group was higher than that in the 24h group or 48h group (P<0.05). At the concentration of IL-1βof 20 ng/ml, the 48h group showed higher levels of BCRP mRNA expression than the 24h group (P<0.05).The expression of BCRP mRNA increased with the increase of IL-1βconcentration. After 48h of IL-1βculture, the 100 ng/ml group showed high levels of BCRP mRNA expression compared with the 0 ng/ml group (P<0.05). After 72h of IL-1βculture, compared with the 0 ng/ml group, the expression of BCRP mRNA was significantly increased in the 20 ng/ml or 50 ng/ml or 100 ng/ml group (P<0.01); and the 100 ng/ml group showed high levels of BCRP mRNA expression compared with the 20 ng/ml group (P < 0.05).ConclusionThe expression of BCRP mRNA in FLS of RA patients has a certain concentration and time dependence of IL-1β, suggesting that IL-1β is involved in BCRP-mediated multidrug resistance, which lays a foundation for exploring its specific mechanism.References[1] Takase-Minegishi K, Horita N, Kobayashi K, et al. Diagnostic test accuracy of ultrasound for synovit...