Objective To determine whether macrophages can behave as antigen presenting cells participating the formation of immunological synapse in rheumatoid arthritis (RA) and whether this process can affect the apoptosis. Moreover, this study was aimed to observe the function of cyclophilin A (CypA) in immunological synapse formation and its role in regulating the apoptosis of macrophages. Methods human acute monocytic leukemia cell line (THP-1) induced macrophages were coated with staphylococcal enterotoxin B(SEB) (100 ng/ml) and co-cultured with activated Jurkat T cells (human acute T-cell leukemia cell line), then incubated in the RPMI-1640 for 16 hours to induce apoptosis. The apoptosis of the macrophages were analyzed by flow cytometry by Annexin V-PI staining. The macrophages cultured in the RPMI-1640 alone were used as control. Meanwhile, CypA (200 ng/ml) were added to or not added in order to observe the apoptosis of macrophages. The function of CypA and the apoptosis of macrophages isolated from RA peripheral blood were also investigated through co-culture with CD4+T cells isolated by immunomagnetic beads. Comparisons between groups were performed by two-sample t-tests. Results In the peripheral blood of healthy people and RA patients, the apoptosis of macrophages which participated immunological synapse was (32.9±2.8)%, (24.7±1.6)%, (14.5±1.2)% respectively, which was significantly lower than the apoptosis of macrophages cultured alone [ respectively for (61.4±2.4)%, (45.5±2.6)%, (22.9±1.5)%, (P<0.05) ]. After CypA was added, the apoptosis of macrophages in cell lines, healthy people and RA patients decreased to (27.2±2.1)%, (20.1±1.1)%, (12.9±1.0)%, lower than the apoptosis of macrophages which participated immunological synapse formation (P<0.05). Conclusion In RA, the macrophages participate in the formation of immunological synapse by interacting with CD4+ T cells. They can significantly reduce the apoptosis on themselves. CypA can enhance this effect. These results provide a new theoretical foundation for prolonged survival of macrophages in RA, which can secrete a variety of cytokines to enhance inflammation and joint destruction.

Objective To detect the levels of procalcitonin in multiple genes autoinflammatory disease (adult Still disease,systemic juvenile idiopathic arthritis,crohn's Crohn's disease),and to explore the relationship between erythrocyte sedimentation rate (ESR),C-reactive protein (CRP),ESR/CRP and disease or complicated infection combined disease.Methods One hundred and fifty-three patients were en-rolled,88 patients with multiple genes autoinflammatory disease,including 32 cases of adult Still disease,27 cases of systemic juvenile idiopathic arthritis,29 cases of Crohn's disease.In addition,30 cases of healthy controls,35 patients with systemic lupus erythematosus (SLE) were included into this study.Electroche-miluminescence was used to test the value of serum PCT,erythrocyte sedimentation rate was tested by blood sedimentation instrument method,the CRP level was tested by lmmunoturbidimetry,and the data was handed managed and analysised by matlab software and One-way analysis of variance (ANOVA) was used to compare the differences of PCTs between groups.Results ① In the non-infection condition,the PCT value of the autoimmune inflammatory diseases [(0.36±0.74) μg/L,95％confidence interval (CI) (0.174 9,0.550 9) μg/L)] was signifieantly higher than that of the healthy control group [(0.06±0.06) μg/L,95％CI (0.035 1,0.081 7 μg/L)],the difference was statistically significant (F=5.03,P=0.027 4),but there was no statistically significant (F=1.03,P=0.475 5) when comparing with SLE group.② The PCT level of the non-infected inflammatory enteric arthritis [(0.20±0.32),95％CI(0.042 7,0.364 3) μg/L] was different compared with the healthy group,the difference was statistically significant (F=5.77,P=0.020 4),at the same time,the difference was not statistically significant when comparing with the SLE group (F=0.22,P=0.647 6).When the PCT value in non-infected adults Still disease [(0.60±1.02) 95％CI(0.048 4,1.153 6) μg/L] compared with the healthy group,the difference was statistically significant (F=7.22,P=0.01) but the difference was not statistically different when compared with the SLE group (F=2.65,P=0.114 3).The PCT level difference was statistically significant (F=2.23,P＜0.01)when comparing infection-free juvenile idiopathic arthritis [(1.52±2.02) μg/L,95％CI(0.054 8,4.591 9) μg/L] and the healthy group,the difference was statistically significantly different (F=8.34,P=0.004 7) when compared with the PCT of the non-infected SLE group.③ In the case of autoinflammatory diseases without infection,the 95％CI of ESR/CRP ratio was between 1.121 2 and 3.589 4.In the case of co-infection,the 95％ CI of ESR/CRP ratio was between 1.502 2 and 8.718 8,so we considered autoimmune inflammatory diseases might had a high possibility of co-infection when the ESR/CRP ratio was higher than 3.5.Conclusion ① The multiple genes autoinflammatory disease group has a higher value of PCT level than healthy controls even without infection.② The mean and 95％CI range of PCT of the inflammatory bowel disease arthritis,adult Still disease and the juvenile id-iopathic arthritis is significantly higher than the healthy controls,partially higher than SLE group.In addition,the PCT level in the juvenile idiopathic arthritis is the highest.③ In clinical,to estimate whether the multiple genes autoinflammatory disease has bacterial infection,we can't just simply rely on PCT to estimate whether the multiple genes autoinflammatory disease has bacterial infection,we may consider the ratio of the ESR/CRP,when the value is higher than 3.5,we may consider patients has strong probability with infection.

Objective:To explore the expression and predictive value of serum CD36 level in cardio-vascular risk in patients with rheumatoid arthritis (RA) and to provide a new theoretical basis for clinical iden-tification and prediction of patients at moderate and high cardiovascular risk in RA patients.Methods:Eighty-four RA patients hospitalized to the Department of Rheumatology and Immunology of the second hospital of Lanzhou University in Gansu Province were selected as the study subjects, and 34 healthy people were selected as the controls. All RA patients were divided into low cardiovascular risk groups and medium and high cardiovascular risk groups according to prediction for ASCVD risk in China (China-PAR) cardiovascular risk assessment. At the same time, they were tested for serological indicators at admission. Statistical Product and Service Solutions (SPSS)) 26.0 software was used for the statistical data analysis. T-test and nonparametric test were used for comparison of the measurement data. The Chi-square test and Fisher's exact test were used for the comparison of classified data. Variables with P<0.05 in univariate analysis were included into the Logistic regression model. Results:Compared with the healthy control group, the number of patients with medium and high cardiovascular risk in RA[8 cases (23.5)% and 38 cases (45.2)%, χ2=4.80, P=0.029] was significantly higher and was negatively correlated with serum CD36 ( r=-0.27, P<0.05). Logistic regression analysis showed that age [ OR(95% CI)=1.654(1.157, 2.365), P=0.006] and diastolic blood pressure [ OR(95% CI)=1.225(1.040, 1.442) , P=0.015] were independent risk factors for medium and high cardiovascular risk in RA patients, and serum CD36 level [ OR(95% CI)=0.569(0.352, 0.922) , P=0.022] was the protective factor of medium and high cardiovascular risk in RA patients according to the results of Logistic regression analysis. The area under the receiver operating characteristic (ROC) area under the curve (AUC) was 0.691, the cut-off value was 4.27 pg/ml, and the sensitivity and specificity were 89.7% and 41.0% respectively. Conclusion:The serum CD36 level decreases with the increase of cardiovascular risk in RA patients. A higher serum CD36 level is a protective factor of cardiovascular risk in RA patients, and CD36 has a certain predictive value for cardiovascular risk in RA patients and is a potential predictor.