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Zeng Q.,Chinese PLA General Hospital | Dong S.-Y.,Chinese PLA General Hospital | Wu L.-X.,Chinese Institute of Aviation Medicine | Li H.,Health Management Center | And 6 more authors.
PLoS ONE | Year: 2013

Background: The presence of food-specific IgG antibodies in human serum may be useful for diagnosis of adverse food reactions. However, the clinical utility of tesing for such antibodies remains very controversial. The aim of this study was to evaluate the serum levels and population distribution of food-specific IgGs and their association with chronic symptoms in a large-scale Chinese population. Methodology/Principal Findings: A total of 21305 adult participants from different regions of China had 14 type of food-specific serum IgG antibodies that were measured by enzyme-linked immunosorbent assay. Amongthese, 5,394 participants were randomly chosen to complete follow-up questionnaire surveys on their dietary characteristics and chronic symptoms. The concentrations of food-specific IgGs against 14 foods ranged from a median (interquartile range) of 7.3 (3.8, 12.6) U/mL of pork-specfic IgG to 42.3 (28.8, 60.2) U/mL of crab-specific IgG. The concentration of food-specific IgGs was closely related to gender; after adjustment for region and age, women had higher concentrations of food-specific IgGs against all of the 14 foods except chicken (regression coefficient (95% CI): 0.01 (-0.003, 0.023); P = 0.129) and corn (0.002 (-0.013, 0.016); P = 0.825). Similar results were also found in the relationship of geographic region to the food-specific IgG concentrations for the 14 foods. Chronic symptoms were negatively associated with the concentrations of a few food-specific IgGs, and were positively associated with the concentrations of other food-specific IgGs. Conclusions: The levels of food-specific IgGs were variable both in healthy and in symptomatic Chinese adults. These findings raise awareness that demographic factors, the type of food and specific chronic symptoms should be considered before food elimination treatment based on IgG testing in patients with chronic symptoms is used in clinical practice. © 2013 Zeng et al. Source

Chen W.W.,Treatment and Research Center for Infectious Diseases
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2012

To investigate the characteristics of γδ T cell subsets in peripheral blood and Vδ1 and Vδ2 T cell subsets proliferation after induction in vitro, and to provide experimental basis for γδ T cells expansion methods in vitro. Percentages of γδ T cells, Vδ1 and Vδ2 T cells in CD3 T cells from 25 cases of HIV/AIDS patients (HIV group) and 31 cases of healthy adults as control (HC group) were investigated with flow cytometry (FCM); and 10 cases peripheral blood mononuclear cells (PBMCs) from each group were induced and cultured for 14 d by using anti-γδ TCR mAb and IL-2, then the cell amounts were counted, γδ T cells and Vδ1, Vδ2 T cells were detected and analyzed with flow cytometry (FCM) at 0 d, 7 d and 14 d. The percentages and absolute counts of γδ T cells and V δ2 T cells in HIV group were significantly lower than those in HC group, but those of Vδ1 subsets were significantly higher than those of HC group. After culture for 14 day, the total cell amount of HC group expanded almost 3 times, but those of HIV group expanded a little; The percentages of γδ T cells in HC group were above 80%, but those in HIV group were only about 35%; the percentages of Vδ2 T cells in HC group were about 65%, but those in HIV group were only about 17%. The proportion of γδ T cells in peripheral blood of HIV/AIDS patients decreased significantly, and Vδ1/Vδ2 ratio was inversed; the expansion effect was not so good to use anti-γδ TCR mAb and IL-2 to induce γδ T cells and Vδ2 subsets of HIV/AIDS, and the Vδ1/Vδ2 ratio inversion could not reverse. More efficient culture methods should be explored. Source

Chen W.,Treatment and Research Center for Infectious Diseases | Hou Z.,Jinan University | Li C.,Jinan University | Xiong S.,Jinan University | Liu H.,Chinese Academy of Agricultural Sciences
PLoS ONE | Year: 2011

Background: Members of the B7 superfamily costimulate the proliferation of lymphocytes during the initiation and maintenance of antigen-specific humoral and cell-mediated immune responses. B7-H3 (CD276) is a newly identified member of the B7 superfamily. It has been shown that B7-H3 plays a significant role in regulating T cell response in humans and mice, but it is not known whether a counterpart of human or murine B7-H3 exists in porcine species. Methodology/Principal Findings: We cloned the porcine 4ig-b7-h3 gene using a blast search at the NCBI database with human b7-h3, RT-PCR and 3′-terminus RACE. Protein sequence analysis showed that the protein encoded by this gene contained 4Ig-like domains and was 90.88% identical with human 4Ig-B7-H3. Results of Dot-blot hybridization and RT-PCR showed that B7-H3 was broadly distributed in porcine tissues mainly as two isoforms, 2Ig-B7-H3 and 4Ig-B7-H3, of which 4Ig-B7-H3 was dominant. We further demonstrated that porcine 4Ig-B7-H3 was able to inhibit the proliferation and cytokine production of porcine T cells activated through the TCR pathway, similar to human B7-H3. Conclusion: We cloned the porcine 4ig-b7-h3 gene and demonstrated that the porcine 4Ig-B7-H3 serves as a negative regulator for the T-cell immune response. © 2011 Hou et al. Source

Fan Y.-C.,Shandong University | Li W.-G.,Treatment and Research Center for Infectious Diseases | Zheng M.-H.,Wenzhou Medical College | Gao W.,Shandong University | And 2 more authors.
Gene | Year: 2012

Invasive fungal infection (IFI) is a life-threatening infection occurring most often in patients with systemic lupus erythematosus (SLE) and few data has been reported in SLE patients particularly in China. This present study was aimed to determine IFI prevalence, associated risk factors and patterns of infection in Chinese SLE patients. A retrospective study was conducted in a single institute of Northern China from July 2004 and October 2010. Demographic characteristics, clinical and laboratory data, and mycological examinations were collected. Among 1534 patients included, 20 (1.6%) were diagnosed with IFI, of whom there were 18 females and 2 males with the average age of 35.4. ±. 15.1. years old. Involved sites included nine lungs, six central nervous system and five disseminated cases. 6 of 20 IFIs cases (30%) were non-survivors including 2 lungs, 2 central nervous system and 2 disseminated cases. Compared with survivors, non-survivors had significantly higher equivalent prednisone doses, elevated level of serum C reactive protein (CRP), higher erythrocyte sedimentation rate (ESR), higher thrombocytopenia rate and higher systemic lupus erythematosus disease activity index (SLEDAI) score. These results strongly demonstrated that prednisone doses, CRP, ESR, thrombocytopenia and SLEDAI could be associated risk factors in the prognosis of SLE patients with IFI. © 2012 Elsevier B.V. Source

Zhang Z.,Research Center for Biological Therapy | Zhang Z.,University of North Carolina at Chapel Hill | Zhang Z.,Research Center for Clinical Medicine | Cheng L.,University of North Carolina at Chapel Hill | And 11 more authors.
Journal of Clinical Investigation | Year: 2015

Group 3 innate lymphoid cells (ILC3s) have demonstrated roles in promoting antibacterial immunity, maintaining epithelial barrier function, and supporting tissue repair. ILC3 alterations are associated with chronic inflammation and inflammatory disease; however, the characteristics and relevant regulatory mechanisms of this cell population in HIV-1 infection are poorly understood due in part to a lack of a robust model. Here, we determined that functional human ILC3s develop in lymphoid organs of humanized mice and that persistent HIV-1 infection in this model depletes ILC3s, as observed in chronic HIV-1-infected patients. In HIV-1-infected mice, effective antiretroviral therapy reversed the loss of ILC3s. HIV-1-dependent reduction of ILC3s required plasmacytoid dendritic cells (pDCs), IFN-I, and the CD95/FasL pathway, as targeted depletion or blockade of these prevented HIV-1-induced ILC3 depletion in vivo and in vitro, respectively. Finally, we determined that HIV-1 infection induces CD95 expression on ILC3s via a pDC-and IFN-I-dependent mechanism that sensitizes ILC3s to undergo CD95/FasL-mediated apoptosis. We conclude that chronic HIV-1 infection depletes ILC3s through pDC activation, induction of IFN-I, and CD95-mediated apoptosis. Source

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