Increased Macroautophagy in Interferon-Gamma-Producing T Cells from Patients with Newly Diagnosed Systemic Lupus Erythematosus / 中华医学杂志(英文版)

<p><b>Background</b>Imbalance of interferon-gamma (IFN-γ), interleukin (IL)-4, and IL-17 producing by T cells is confirmed to contribute to the pathogenesis of systemic lupus erythematosus (SLE). Autophagy is now emerging as a core player in the development and the function of the immune system. Therefore, we investigated the autophagic behavior in IFN-γ-, IL-4-, and IL-17-producing T cells from patients with SLE.</p><p><b>Methods</b>Thirty patients with SLE and 25 healthy controls matched for gender and age were recruited between September 2016 and May 2017. The autophagic levels in IFN-γ T cells, IL-4 T cells, and IL-17 T cells from patients with newly diagnosed SLE and healthy controls were measured using flow cytometry. The plasma levels of IFN-γ were determined by enzyme-linked immunosorbent assay in SLE patients and healthy controls. Unpaired t-tests and the nonparametric Mann-Whitney U-test were used to compare data from patients with SLE and controls. Spearman's rank correlation coefficient was applied for calculation of the correlation between parallel variables in single samples.</p><p><b>Results</b>Our results showed increased percentage of autophagy in IFN-γ T cells from patients with SLE and healthy controls ([8.07 ± 2.72]% vs. [3.76 ± 1.67]%, t = 5.184, P < 0.001), but not in IL-4 T cells or IL-17 T cells (P > 0.05) as compared to healthy donors. Moreover, the plasma levels of IFN-γ in SLE patients were significantly higher than those in healthy controls ([68.9 ± 29.1] pg/ml vs. [24.7 ± 17.6] pg/ml, t = 5.430, P < 0.001). Moreover, in SLE patients, the percentage of autophagy in IFN-γ T cells was positively correlated with the plasma levels of IFN-γ (r = 0.344, P = 0.046), as well as the disease activity of patients with SLE (r = 0.379, P = 0.039).</p><p><b>Conclusion</b>The results indicate that autophagy in IFN-γ T cells from SLE patients is activated, which might contribute to the persistence of T cells producing IFN-γ, such as Th1 cells, and consequently result in the high plasma levels of IFN-γ, and then enhance the disease activity of SLE.</p>

Detecting anti-megakaryocyte antibodies in serum of systemic lupus erythematosus patients by indirect immunofluorescence / 中国实验血液学杂志

This study was purposed to investigate the mechanism of thrombocytopenia in patients with systemic lupus erythematosus (SLE) through detecting anti-megakaryocyte antibodies in SLE patients. The serum anti-megakaryocyte antibodies in 36 SLE cases with thrombocytopenia were detected by using indirect immunofluorescence, the detected results were compared with detected results of 30 SLE cases without thrombocytopenia and 30 healthy persons. The results showed that the positive incidences of anti-megakaryocyte antibody in serum of 36 SLE cases with thrombocytopenia, 30 SLE cases without thrombocytopenia and 30 healthy persons were 19.4% (7/36), 6.7% (2/30) and 3.3% (1/30) respectively. As compared with SLE patients without thrombocytopenia and healthy persons, SLE patients with thrombocytopenia had higher incidence of anti-megakaryocyte antibodies, moreover there was significant difference between SLE patients with thrombocytopenia and healthy persons (p < 0.05), while there was no significant difference between SLE patients with or without thrombocytopenia (p > 0.05). It is concluded that autoantibodies against megakaryocytes exist in SLE patients and may partially contribute to the incidence of thrombocytopenia in SLE patients. The detection of anti-megakaryocyte antibodies with a enough case number is needed to make a final conclusion on thrombocytopenia pathogenesis in SLE.

Anti-EPO receptor antibodies in systemic lupus erythematosus with anemia / 中华风湿病学杂志

Objective To investigate the presentationand significance of circulating autoantibodies to erythropoietin receptor (EPOR) in sera from patients with systemic lupus erythematosus (SLE). Methods One hundred and twenty-four consecutive patients with SLE, seven with autoimmune hemolytic anemia (AIHA), 19 patients with iron deficiency anemia (IDA) and 45 normal individuals were involved in this study. In all patients with SLE, the disease activity was evaluated using the European consensus Lupus Activity Measurement scale. Antibodies to EPOR were detected by enzyme-linked immunosorbent assay (ELISA). All data were tested with Chi-squared or Student's t tests by SPSS software. Results A higher frequency of antibodies to EPOR were detected in SLE patients than healthy controls (20.2% vs 2.2%, P=0.004), however, they could not be detected in AIHA and IDA patients. Moreover, anti-EPOR antibodies were detected in 17 (33.3%) of 51 SLE patients with anemia, compared with that in 8 (11.0%, P=0.002) of 73 patients without anemia. Furthermore, patients with antibodies to EPOR had more severe anemia and often presented as microcytic anemia (P =0.005) than those without anti-EPOR antibodies. Finally, anti-EPOR antibodies seemed to be more likely to occur in patients with skin rash (P=0.014), low levels of C3 component of complement (P=0.01), positive anti-dsDNA antibodies (P=0.000) and higher disease activity scores (P= 0.024). Conclusion The higher incidence of antibodies to EPOR in SLE patients with anemia suggest that anti-EPOR antibodies might play a vital role in the development of anemia in SLE patients. Thus, detecting anti-EPOR antibodies in SLE patients with anemia may be helpful.

Expression of FLICE-inhibitory protein in synovial tissue and its association with synovial inflammation in juvenile idiopathic arthritis / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To examine the expression of FLICE-inhibitory protein (FLIP) in juvenile idiopathic arthritis (JIA) and analyze its correlation with synovial inflammation.</p><p><b>METHODS</b>The expression of FLIP was assessed in 11 JIA and 3 normal synovial tissue samples by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. The cell types expressing FLIP were further characterized, and the correlation of FLIP expression with the degree of synovial inflammation, as well as the activity of caspase 8 was then analyzed.</p><p><b>RESULTS</b>RT-PCR revealed the expression of FLIP mRNA in all 11 JIA samples, but not in 3 normal synovial tissues. In JIA, FLIP expression could be found in both the lining and sublining layers, mainly in the macrophage-like cells. Moreover, the expression of FLIP in JIA synovial tissues was positively correlated with the degree of synovial inflammation (r = 0.563, P < 0.05).</p><p><b>CONCLUSION</b>The expression of antiapoptotic FLIP in JIA synovial tissue and its correlation to accumulation of inflammatory cells in synovial tissue suggests that FLIP potentially extends the lifespan of synovial cells and thus contributes to the progression of joint destruction.</p>