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      CD40 up-regulation on dendritic cells correlates with Th17/Treg imbalance in chronic periodontitis in young population

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          Abstract

          We aimed to discover the influence of age on the development of chronic periodontitis and illustrate the molecular mechanism in this process. Blood samples were collected from 63 chronic periodontitis patients and 30 healthy controls. Th17 cell/Foxp3 + regulatory T cell (Treg) ratio and expression of costimulatory molecules in dendritic cells (DCs) were analyzed by flow cytometry. The serum levels of soluble CD40 ligand (CD40L) and IL-17 were examined by ELISA. In young chronic periodontitis patients, the Th17/Treg ratio was significantly higher than that in old patients. CD40 on DCs and serum levels of CD40L and IL-17 were all higher in young chronic periodontitis patients. Mature DCs with high CD40 expression level elevated the Th17/Treg ratio in vitro. During the pathogenesis of chronic periodontitis, young patients had higher Th17/Treg ratio than old patients and this phenomenon was in line with the differential expression levels of CD40 in DCs.

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          Inflammatory and immune pathways in the pathogenesis of periodontal disease.

          The pathogenesis of periodontitis involves a complex immune/inflammatory cascade that is initiated by the bacteria of the oral biofilm that forms naturally on the teeth. The susceptibility to periodontitis appears to be determined by the host response; specifically, the magnitude of the inflammatory response and the differential activation of immune pathways. The purpose of this review was to delineate our current knowledge of the host response in periodontitis. The role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered. New information relating to regulation of both inflammation and the immune response will be reviewed in the context of susceptibility to, and perhaps control of, periodontitis. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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            Cytokines that promote periodontal tissue destruction.

            Although periodontal diseases are initiated by bacteria that colonize the tooth surface and gingival sulcus, the host response is believed to play an essential role in the breakdown of connective tissue and bone, key features of the disease process. An intermediate mechanism that lies between bacterial stimulation and tissue destruction is the production of cytokines, which stimulates inflammatory events that activate effector mechanisms. These cytokines can be organized as chemokines, innate immune cytokines, and acquired immune cytokines. Although they were historically identified as leukocyte products, many are also produced by a number of cell types, including keratinocytes, resident mesenchymal cells (such as fibroblasts and osteoblasts) or their precursors, dendritic cells, and endothelial cells. Chemokines are chemotactic cytokines that play an important role in leukocyte recruitment and may directly or indirectly modulate osteoclast formation. This article focuses on aspects of osteoimmunology that affect periodontal diseases by examining the role of cytokines, chemokines, and immune cell mediators. It summarizes some of the key findings that attempt to delineate the mechanisms by which immune factors can lead to the loss of connective tissue attachment and alveolar bone. In addition, a discussion is presented on the importance of clarifying the process of uncoupling, a process whereby insufficient bone formation occurs following resorption, which is likely to contribute to net bone loss in periodontal disease.
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              Heterogeneity of CD4+ memory T cells: functional modules for tailored immunity.

              Phenotypic and functional heterogeneity is the hallmark of effector and memory T cells. Upon antigenic stimulation, naïve CD4(+) T cells make choices to become effector Th1, Th2 or Th17 cells, or even Treg. In addition to differences in cytokine repertoire, effector CD4(+) T cells exhibit diversity in homing, such as migration to lymph node follicles to help B cells versus migration to inflamed tissues. Upon clearance of the antigen, two major types of memory T cells remain: central memory cells, which patrol lymphoid organs, and effector memory cells that act as sentinels in peripheral tissues such as the skin and the gut. Here, we review our current understanding of CD4(+) T-cell lineage heterogeneity and flexibility, with emphasis on the human system, and propose an organization of effector and memory T cells based on distinct functional modules.
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                Author and article information

                Journal
                Innate Immun
                Innate Immun
                INI
                spini
                Innate Immunity
                SAGE Publications (Sage UK: London, England )
                1753-4259
                1753-4267
                28 April 2020
                August 2020
                : 26
                : 6
                : 482-489
                Affiliations
                [1-1753425920917731]Department of Stomatology, Fourth Affiliated Hospital of Harbin Medical University, China
                Author notes
                [*]Xin Su, Department of Stomatology, Fourth Affiliated Hospital of Harbin Medical University, No. 37 Summer Palace Street, Nangang District, Harbin 150001, Heilongjiang, China. Email: suxin13845139401@ 123456sina.com
                Author information
                https://orcid.org/0000-0002-0366-270X
                Article
                10.1177_1753425920917731
                10.1177/1753425920917731
                7491239
                32345091
                ff76e142-00b2-45a5-b4aa-75c3da8f1bef
                © The Author(s) 2020

                Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 17 December 2019
                : 27 February 2020
                Funding
                Funded by: the Joint Guidance Project of Heilongjiang Natural Science Foundation;
                Award ID: LH2019H075
                Categories
                Original Articles
                Custom metadata
                ts2

                Immunology
                chronic periodontitis,th17 cells,regulatory t cells,dendritic cells,cd40 up-regulation
                Immunology
                chronic periodontitis, th17 cells, regulatory t cells, dendritic cells, cd40 up-regulation

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