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      Circulating memory B cells and plasmablasts are associated with the levels of serum immunoglobulin in patients with ulcerative colitis

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          Abstract

          Humoural immunity is crucial for the pathogenesis of ulcerative colitis ( UC), but the precise perturbation of B cell immunity is poorly understood. This study is aimed at evaluating the numbers of different subsets of circulating memory B cells, plasmablasts, and the levels of serum immunoglobulin in UC patients. Total of 23 patients with active UC and 14 healthy controls ( HC) were examined for the numbers of different subsets of circulating memory B cells and plasmablasts before and after treatment with mesalazine for 8–12 weeks by flow cytometry. Disease activity was evaluated by the Mayo clinic score. The levels of serum immunoglobulin, C‐reactive protein ( CRP) and erythrocyte sedimentation rate ( ESR) were measured in individual subjects. In comparison with that in HC, significantly reduced numbers of IgG + IgD   CD27 +  CD19 + memory B cells, increased numbers of CD20   CD19 + plasmablast subsets, and higher serum IgG levels were detected in UC patients. The concentrations of serum IgG, the numbers of CD138 +  CD38 +  CD20   CD19 +, and IgG +  CD38 +  CD20   CD19 + plasmablasts were negatively associated with the numbers of IgG + IgD   CD27 +  CD19 + memory B cells. Furthermore, the values of Mayo clinic score, CRP, or ESR in UC patients were negatively correlated with the numbers of IgG + IgD   CD27 +  CD19 + memory B cells, while positively correlated with the serum IgG levels and the numbers of plasmablast subsets. Following treatment with mesalazine, the numbers of circulating IgG + IgD   CD27 +  CD19 + memory B cells were significantly increased, while the numbers of CD138 +  CD38 +  CD20   CD19 + and IgG +  CD38 +  CD20   CD19 + plasmablasts were reduced in UC patients. These decreased IgG + IgD   CD27 +  CD19 + memory B cells and increased plasmablasts may be involved in the pathogenic process of UC.

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          Most cited references30

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          Standardizing immunophenotyping for the Human Immunology Project.

          The heterogeneity in the healthy human immune system, and the immunological changes that portend various diseases, have been only partially described. Their comprehensive elucidation has been termed the 'Human Immunology Project'. The accurate measurement of variations in the human immune system requires precise and standardized assays to distinguish true biological changes from technical artefacts. Thus, to be successful, the Human Immunology Project will require standardized assays for immunophenotyping humans in health and disease. A major tool in this effort is flow cytometry, which remains highly variable with regard to sample handling, reagents, instrument setup and data analysis. In this Review, we outline the current state of standardization of flow cytometry assays and summarize the steps that are required to enable the Human Immunology Project.
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            Innate and adaptive immunity in inflammatory bowel disease.

            Inflammatory bowel disease (IBD) includes Crohn's disease (CD) and ulcerative colitis (UC). The exact cause of IBD remains unknown. Available evidence suggests that an abnormal immune response against the microorganisms of the intestinal flora is responsible for the disease in genetically susceptible individuals. The adaptive immune response has classically been considered to play a major role in the pathogenesis of IBD. However, recent advances in immunology and genetics have clarified that the innate immune response is equally as important in inducing gut inflammation in these patients. In particular, an altered epithelial barrier function contributes to intestinal inflammation in patients with UC, while aberrant innate immune responses, such as antimicrobial peptide production, innate microbial sensing and autophagy are particularly associated to CD pathogenesis. On the other hand, besides T helper cell type (Th)1 and Th2 immune responses, other subsets of T cells, namely Th17 and regulatory T (Treg) cells, are likely to play a role in IBD. However, given the complexity and probably the redundancy of pathways leading to IBD lesions, and the fact that Th17 cells may also have protective functions, neutralization of IL-17A failed to induce any improvement in CD. Studying the interactions between various constituents of the innate and adaptive immune systems will certainly open new horizons in the knowledge about the immunologic mechanisms implicated in gut inflammation. Copyright © 2013 Elsevier B.V. All rights reserved.
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              Recent advances in inflammatory bowel disease: mucosal immune cells in intestinal inflammation.

              The intestine and its immune system have evolved to meet the extraordinary task of maintaining tolerance to the largest, most complex and diverse microbial commensal habitat, while meticulously attacking and containing even minute numbers of occasionally incoming pathogens. While our understanding is still far from complete, recent studies have provided exciting novel insights into the complex interplay of the many distinct intestinal immune cell types as well as the discovery of entirely new cell subsets. These studies have also revealed how proper development and function of the intestinal immune system is dependent on its specific microbiota, which appears to have evolutionarily co-evolved. Here we review key immune cells that maintain intestinal homeostasis and, conversely, describe how altered function and imbalances may lead to inflammatory bowel disease (IBD). We highlight the latest developments within this field, covering the major players in IBD including intestinal epithelial cells, macrophages, dendritic cells, adaptive immune cells, and the newly discovered innate lymphoid cells, which appear of characteristic importance for immune function at mucosal surfaces. We set these mucosal immune pathways in the functional context of IBD risk genes where such insight is available. Moreover, we frame our discussion of fundamental biological pathways that have been elucidated in model systems in the context of results from clinical trials in IBD that targeted key mediators secreted by these cells, as an attempt of 'functional' appraisal of these pathways in human disease.
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                Author and article information

                Journal
                J Cell Mol Med
                J. Cell. Mol. Med
                10.1111/(ISSN)1582-4934
                JCMM
                Journal of Cellular and Molecular Medicine
                John Wiley and Sons Inc. (Hoboken )
                1582-1838
                1582-4934
                22 January 2016
                May 2016
                : 20
                : 5 ( doiID: 10.1111/jcmm.2016.20.issue-5 )
                : 804-814
                Affiliations
                [ 1 ] Department of Central Laboratory The First HospitalJilin University ChangchunChina
                [ 2 ] Key Laboratory of Zoonosis Research Ministry of Education The First HospitalJilin University ChangchunChina
                [ 3 ]Jiangsu Co‐innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses YangzhouChina
                [ 4 ] Department of Radiation OncologyChina‐Japan Union Hospital of Jilin University ChangchunChina
                Author notes
                [*] [* ] Correspondence to: Dr. Pujun GAO.

                E‐mail: pujungao@ 123456yeah.net

                [†]

                These authors made equal contributions to this study.

                Article
                JCMM12728
                10.1111/jcmm.12728
                4831367
                26800315
                35450437-ee3d-4906-a4cb-9c726f53b2fa
                © 2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 13 May 2015
                : 29 September 2015
                Page count
                Pages: 11
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 30972610
                Award ID: 81273240
                Funded by: Jilin Province Science and Technology Agency
                Award ID: 20110716
                Funded by: Health Department Research Projects of Jilin Province
                Award ID: 2009Z054
                Award ID: 2013Z026
                Funded by: Norman Bethune Program of Jilin University
                Award ID: 2012206
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                jcmm12728
                May 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.8.6 mode:remove_FC converted:09.04.2016

                Molecular medicine
                ulcerative colitis,memory b cells,plasmablasts,igg
                Molecular medicine
                ulcerative colitis, memory b cells, plasmablasts, igg

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