Key Laboratory of Rheumatology and Clinical Immunology

Beijing, China

Key Laboratory of Rheumatology and Clinical Immunology

Beijing, China
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Deng C.,Peking Union Medical College | Deng C.,Key Laboratory of Rheumatology and Clinical Immunology | Zhang S.,Peking Union Medical College | Zhang S.,Key Laboratory of Rheumatology and Clinical Immunology | And 16 more authors.
PLoS ONE | Year: 2017

Background A reference interval (RI) for the circulating concentration of anti-dsDNA antibody is essential for clinicians to interpret laboratory results and make clinical decisions. Therefore, we aimed to establish the RI for anti-dsDNA antibody in the Chinese Han population. Methods This study was designed and carried out in accordance with guideline C28-A3, which is proposed by the International Federation of Clinical Chemistry and the Clinical and Laboratory Standards Institute. A total of 2,880 apparently healthy individuals were enrolled using a posteriori sampling. These individuals were recruited from four hospitals, representing the Han populations of north, south, east, and west China. Serum anti-dsDNA antibody levels were measured using the three analytical systems AESKU, EUROIMMUNE, and INOVA, which are the most commonly used systems in China. Individuals were stratified by gender, age, and region, and the RIs were obtained by nonparametric methods. Results Gender-specific RIs for serum anti-dsDNA antibody in the Chinese Han population were established. Conclusion This is the first exploration of the RI for anti-dsDNA antibody in the Chinese Han population. We have established gender-specific RIs for each assay method commonly used in China. © 2017 Deng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Wu Z.,Peking Union Medical College | Wu Z.,Key Laboratory of Rheumatology and Clinical Immunology | Zhang S.,Peking Union Medical College | Zhang S.,Key Laboratory of Rheumatology and Clinical Immunology | And 16 more authors.
Clinical Rheumatology | Year: 2017

Monocytes are an important component in the innate immune system. However, studies to date have failed to conclude whether their levels are altered in patients with systemic lupus erythematosus (SLE). We applied the cytodiff counting method and comprehensively measured the circulating levels of distinct white blood cell (WBC) subsets, including CD16+, CD16−, and total monocytes, in 61 SLE patients as well as in 203 age-matched healthy controls (HCs). The absolute number of CD16− monocytes, total monocytes, immature granulocytes, mature neutrophils, total neutrophils, and T cell blasts was significantly higher, that of non-cytotoxic T lymphocytes, cytotoxic T + NK lymphocytes, T + NK lymphocytes, total lymphocytes, basophils, and eosinophils significantly lower (all p < 0.05), but that of CD16+ monocytes, B lymphocytes, B cell blasts, non-B and non-T cell blasts, and total blasts was not statistically different in SLE patients, as compared to HC. Specifically, among all subsets examined, the percentage of CD16− monocytes and total monocytes was the only one that could discriminate active SLE from quiescent SLE (p = 0.033 and 0.026, respectively). SLE patients with lupus nephritis were also associated with higher levels of circulating CD16− monocytes and total monocytes, in comparison with that of controls (both p < 0.0001). This study suggests the significance of distinct WBC subsets, particularly the differential regulations of monocyte subsets, in the pathogenesis and development of SLE. © 2017 International League of Associations for Rheumatology (ILAR)

Xu L.,Tsinghua University | Xu L.,Peking Union Medical College | Li G.,Tsinghua University | Li G.,Peking Union Medical College | And 20 more authors.
Journal of Immunology | Year: 2014

B cell activation is regulated through the interplay of the BCR with the inhibitory coreceptor FcγRIIB and the activating coreceptor CD19. Recent studies suggest that Ag-driven BCR microclusters are efficiently converted to a signaling active state on colocalization with CD19 microclusters. Using total internal reflection fluorescence microscopy-based, high-resolution, highspeed live-cell and molecule imaging approaches, we show that when co-ligated to the BCR, the FcγRIIB can inhibit B cell activation by blocking the colocalization of BCR and CD19 microclusters within the B cell immunological synapse. Remarkably, this inhibitory function of FcgRIIB is dependent not on its well-characterized ITIM-containing cytoplasmic domain, but its transmembrane domain. Indeed, human primary B cells from systemic lupus erythematosus patients homozygous for gene encoding the loss-of-function transmembrane domain mutant FcγRIIB-I232T fail to block the synaptic colocalization of the BCR with CD19, leading to dysregulated recruitment of downstream signaling molecule p-PI3K to membrane proximal signalosome. This inhibitory function of FcγRIIB in impairing the spatial-temporal colocalization of BCR and CD19 microclusters in the B cell immunological synapse may help explain the hyper-reactive features of systemic lupus erythematosus patient B cells in reported studies. These observations may also provide new targets for therapies for systemic autoimmune disease. Copyright © 2014 by The American Association of Immunologists, Inc.

Peng L.,Peking Union Medical College | Peng L.,Key Laboratory of Rheumatology and Clinical Immunology | Ma W.,Peking University | Yi F.,Peking University | And 13 more authors.
Journal of Rheumatology | Year: 2014

Objective. Characterized by chronic inflammation, dysfunction of exocrine glands, and systemic autoimmunity, primary Sjögren syndrome (pSS) is a common autoimmune disease in elderly women. Our study was performed to explore the potential involvement of microRNA (miRNA) in Chinese patients with pSS. Methods. Using microarrays, miRNA expression in peripheral blood mononuclear cells (PBMC) was profiled in 4 female patients with pSS and 3 healthy participants, followed by a large-scale study of 33 patients and 10 healthy individuals. Compared to the healthy participants, 202 miRNA were upregulated and 180 were downregulated in the patients with pSS. To confirm this finding, a set of regulated miRNA was further examined in a large patient group, using quantitative reverse transcriptase-PCR assays. Results. MiR-181a was the miRNA that most profoundly differed between patients with pSS and healthy individuals; however, similar miRNA-181a expression profiles were found in groups with different disease phenotypes. Together, these observations suggested that an elevated miRNA-181a level is a general phenomenon in Chinese patients with pSS. Conclusion. In addition to the elevated miR-181a levels, our study led to the speculation that elevated miR-181a levels in the PBMC of these patients compromise the maturation of B cells, enabling them to recognize and attack autoantigens and resulting in disease phenotypes. In addition to the regulation of human miRNA, many virus-derived miRNA were unexpectedly upregulated in the patients with pSS, suggesting that viral infection of PBMC plays a role in this disease. Copyright © 2014. All rights reserved.

Xu L.,Tsinghua University | Xu L.,Collaborative Innovation Center for Infectious Diseases | Xu L.,Peking Union Medical College | Xu L.,Key Laboratory of Rheumatology and Clinical Immunology | And 12 more authors.
Journal of Leukocyte Biology | Year: 2015

Sphingolipid- and cholesterol-rich lipid raft microdomains are important in the initiation of BCR signaling. Although it is known that lipid rafts promote the coclustering of BCR and Lyn kinase microclusters within the B cell IS, the molecular mechanism of the recruitment of lipid rafts into the B cell IS is not understood completely. Here, we report that the synaptic recruitment of lipid rafts is dependent on the cytoskeleton-remodeling proteins, RhoA and Vav. Such an event is also efficiently regulated by motor proteins, myosin IIA and dynein. Further evidence suggests the synaptic recruitment of lipid rafts is, by principle, an event triggered by BCR signaling molecules and second messenger molecules. BCR-activating coreceptor CD19 potently enhances such an event depending on its cytoplasmic Tyr421 and Tyr482 residues. The enhancing function of the CD19-PI3K module in synaptic recruitment of lipid rafts is also confirmed in human peripheral blood B cells. Thus, these results improve our understanding of the molecular mechanism of the recruitment of lipid raft microdomains in B cell IS. © Society for Leukocyte Biology.

Chen Z.,Peking Union Medical College | Chen Z.,Key Laboratory of Rheumatology and Clinical Immunology | Chen Z.,Fujian Medical University | Li M.-T.,Peking Union Medical College | And 15 more authors.
Clinical Rheumatology | Year: 2015

With this study, we provide insight into the clinical characteristics, laboratory characteristics, and organ damage associated with incomplete lupus syndromes (ILE) and search for predictors of organ damage in ILE. A retrospective chart review was performed on 77 hospitalized patients with ILE. The control patient group comprised 2104 systemic lupus erythematosus (SLE) patients who were entered into the Chinese SLE Treatment and Research group (CSTAR). The Systemic Lupus International Collaborating Clinics (SLICC)/ACR Damage Index (SDI) was used to classify damage features. Based on their SDI score, ILE patients were divided into SDI > 0 and SDI = 0 groups. The percentages of anti-SSA-seropositive (54.5 %) and anti-RNP-seropositive (24.7 %) patients with ILE were higher than those found among the SLE patients from CSTAR (p < 0.001). The mean SDI score was 0.66 (range 0–2), and a damage score greater than 0 was present in 41 (53.3 %) patients. The most prevalent damage category was pulmonary damage, present in 17 (22.1 %) patients. Peripheral vascular damage occurred in individuals who were significantly older than those who had musculoskeletal damage (p = 0.031). The subgroup with SDI > 0 had a higher mean age (36.8 ± 2.04 years) than those with SDI = 0 (30.8 ± 2.08 years; p = 0.044). The mean SLEDAI score in the SDI > 0 patient group (8.2 ± 0.74) was higher than that of the SDI = 0 group (4.8 ± 0.54; p = 0.001). ILE patients may include a subset that is likely to experience progressive organ damage. Organ damage was more common in patients of older age and with high SLEDAI scores. © 2015, International League of Associations for Rheumatology (ILAR).

Xianbin W.,Peking Union Medical College | Xianbin W.,Key Laboratory of Rheumatology and Clinical Immunology | Xianbin W.,Yantai Yuhuangding Hospital | Mingyu W.,Peking Union Medical College | And 10 more authors.
Medicine (United States) | Year: 2015

This article aims to analyze the frequency and clinical characteristics of peripheral neuropathy (PN) in patients with systemic lupus erythematosus (SLE). A total of 4924 SLE patients admitted to the Peking Union Medical College Hospital, Beijing, China, from January 1995 to September 2013 were included in this retrospective analysis. The individuals designated as control patients were selected from the pool of SLE patients without PN using the systematic sampling method of 1:2 during the same time. The prevalence of SLE-associated PN (SLE-PN) in SLE patients was 1.5% (73/4924). Seventy-nine cases of PN affected 73 patients and 6 of these patients (8.2%) presented with 2 types of PN. Among the 7 types of PN, polyneuropathy was the most frequent and was diagnosed in 47 cases (59.5%); the remaining patients suffered from mononeuropathy (13.9%), cranial neuropathy (12.7%), myasthenia gravis (10.1%), autonomic neuropathy (2.5%), or acute inflammatory demyelinating polyradiculoneuropathy (1.3%). Five patients developed PN before the onset of SLE (3 out of 5 patients had myasthenia gravis). The most common PN-related symptoms were myasthenia and numbness (50.6%), followed by pain in affected regions (35.9%). PN symptoms were relieved in a majority of the patients (76.7%) after treatment. Compared with non-SLE-PN patients, patients with SLE-PN had a higher frequency of fever (65.8% vs 45.9%, P<0.01), mucocutaneous involvement (73.9% vs 36.3%, P<0.01), arthritis (42.5% vs 28.1%, P<0.05), myositis (17.8% vs 5.5%, P<0.01), and central nervous system involvement (38.4% vs 21.9%, P<0.05) as well as being positive for the anti-Sm antibody (31.4% vs 18.8%), immunoglobulin G (IgG) elevation (53.6% vs 37.1%, P<0.01), and reduction in complement 3 (54.8% vs 36.9%, P<0.05). A statistically significant difference was found between the Systemic Lupus Erythematosus Disease Activity Index scores in SLE-PN patients compared with the non-SLE-PN patients (P<0.05). Multivariate logistic regression showed that the only risk factor for PN was IgG elevation (odds ratio=2.553, 1.224-5.327, P=0.012). The prevalence of PN in SLE occurs more frequently in patients with an active form of the disease. IgG elevation is a risk factor for SLE-PN and should be assessed in these patients. Young female patients with myasthenia gravis should be closely monitored for the development of SLE. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Zhang L.-N.,Peking Union Medical College | Zhang L.-N.,Key Laboratory of Rheumatology and Clinical Immunology | Shi T.-Y.,Peking Union Medical College | Shi T.-Y.,Key Laboratory of Rheumatology and Clinical Immunology | And 37 more authors.
Hepatology | Year: 2013

The biochemical response to ursodeoxycholic acid (UDCA) in primary biliary cirrhosis is a strong predictor of long-term outcome and thus facilitates the rapid identification of patients needing new therapeutic approaches. Numerous criteria for predicting outcome of treatment have been studied based on biochemical response to UDCA at 1 year. We sought to determine whether an earlier biochemical response at 3 or 6 months could as efficiently identify patients at risk of poor outcome, as defined by liver-related death, liver transplantation, and complications of cirrhosis. We analyzed the prospectively collected data of 187 patients with a median follow-up of 5.8 years (range, 1.3-14 years). The survival rates without adverse outcome at 5 years and 10 years were 86% and 63%. Under UDCA therapy, laboratory liver parameters experienced the most prominent improvement in the first 3 months (P < 0.0001) and then stayed relatively stable for the following months. The Paris, Barcelona, Toronto, and Ehime definitions, but not the Rotterdam definition, applied at 3, 6, and 12 months significantly discriminated the patients in terms of long-term outcome. Compared with biochemical responses evaluated after 1 year of UDCA therapy, biochemical responses at the third month demonstrated higher positive predictive value (PPV) but lower negative predictive value (NPV) and increased negative likelihood ratio (NLR) by all definitions; biochemical responses at the sixth month showed higher or the same PPV and NPV and lower NLR by all definitions. Conclusion: For the previously published criteria, biochemical responses at the sixth month can be used in place of those evaluated after 1 year of UDCA therapy. Our findings justify a more rapid identification of patients who need new therapeutic approaches. © 2013 American Association for the Study of Liver Diseases.

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