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NK-CD11c+ Cell Crosstalk in Diabetes Enhances IL-6-Mediated Inflammation during Mycobacterium tuberculosis Infection
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نویسنده
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cheekatla s.s. ,tripathi d. ,venkatasubramanian s. ,nathella p.k. ,paidipally p. ,ishibashi m. ,welch e. ,tvinnereim a.r. ,ikebe m. ,valluri v.l. ,babu s. ,kornfeld h. ,vankayalapati r.
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منبع
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plos pathogens - 2016 - دوره : 12 - شماره : 10
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چکیده
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In this study,we developed a mouse model of type 2 diabetes mellitus (t2dm) using streptozotocin and nicotinamide and identified factors that increase susceptibility of t2dm mice to infection by mycobacterium tuberculosis (mtb). all mtb-infected t2dm mice and 40% of uninfected t2dm mice died within 10 months,whereas all control mice survived. in mtb-infected mice,t2dm increased the bacterial burden and pro- and anti-inflammatory cytokine and chemokine production in the lungs relative to those in uninfected t2dm mice and infected control mice. levels of il-6 also increased. anti-il-6 monoclonal antibody treatment of mtb-infected acute- and chronic-t2dm mice increased survival (to 100%) and reduced pro- and anti-inflammatory cytokine expression. cd11c+ cells were the major source of il-6 in mtb-infected t2dm mice. pulmonary natural killer (nk) cells in mtb-infected t2dm mice further increased il-6 production by autologous cd11c+ cells through their activating receptors. anti-nk1.1 antibody treatment of mtb-infected acute-t2dm mice increased survival and reduced pro- and anti-inflammatory cytokine expression. furthermore,il-6 increased inflammatory cytokine production by t lymphocytes in pulmonary tuberculosis patients with t2dm. overall,the results suggest that nk-cd11c+ cell interactions increase il-6 production,which in turn drives the pathological immune response and mortality associated with mtb infection in diabetic mice. © 2016 public library of science. all rights reserved.
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آدرس
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department of pulmonary immunology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, department of pulmonary immunology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, department of pulmonary immunology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, national institutes of health,international center for excellence in research,chennai, India, department of pulmonary immunology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, department of cellular and molecular biology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, department of pulmonary immunology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, department of pulmonary immunology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, department of cellular and molecular biology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States, blue peter research center,lepra society,cherlapally,hyderabad, India, national institutes of health,international center for excellence in research,chennai, India, department of medicine,university of massachusetts medical school,worcester,ma, United States, department of pulmonary immunology,center for biomedical research,university of texas health science center at tyler,tyler,tx, United States
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Authors
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