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      Role of T Lymphocytes in Type 2 Diabetes and Diabetes-Associated Inflammation

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      Author(s): 1 , 2 , 2 , 2 , *
      Publication date (Electronic):
      Journal: Journal of Diabetes Research
      Publisher: Hindawi Publishing Corporation

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          Abstract

          Although a critical role of adaptive immune system has been confirmed in driving local and systemic inflammation in type 2 diabetes and promoting insulin resistance, the underlying mechanism is not completely understood. Inflammatory regulation has been focused on innate immunity especially macrophage for a long time, while increasing evidence suggests T cells are crucial for the development of metabolic inflammation and insulin resistance since 2009. There was growing evidence supporting the critical implication of T cells in the pathogenesis of type 2 diabetes. We will discuss the available effect of T cells subsets in adaptive immune system associated with the procession of T2DM, which may unveil several potential strategies that could provide successful therapies in the future.

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          Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance.

          Justin Odegaard, Roberto Ricardo-Gonzalez, Matthew H Goforth … (2007)
          Obesity and insulin resistance, the cardinal features of metabolic syndrome, are closely associated with a state of low-grade inflammation. In adipose tissue chronic overnutrition leads to macrophage infiltration, resulting in local inflammation that potentiates insulin resistance. For instance, transgenic expression of Mcp1 (also known as chemokine ligand 2, Ccl2) in adipose tissue increases macrophage infiltration, inflammation and insulin resistance. Conversely, disruption of Mcp1 or its receptor Ccr2 impairs migration of macrophages into adipose tissue, thereby lowering adipose tissue inflammation and improving insulin sensitivity. These findings together suggest a correlation between macrophage content in adipose tissue and insulin resistance. However, resident macrophages in tissues display tremendous heterogeneity in their activities and functions, primarily reflecting their local metabolic and immune microenvironment. While Mcp1 directs recruitment of pro-inflammatory classically activated macrophages to sites of tissue damage, resident macrophages, such as those present in the adipose tissue of lean mice, display the alternatively activated phenotype. Despite their higher capacity to repair tissue, the precise role of alternatively activated macrophages in obesity-induced insulin resistance remains unknown. Using mice with macrophage-specific deletion of the peroxisome proliferator activated receptor-gamma (PPARgamma), we show here that PPARgamma is required for maturation of alternatively activated macrophages. Disruption of PPARgamma in myeloid cells impairs alternative macrophage activation, and predisposes these animals to development of diet-induced obesity, insulin resistance, and glucose intolerance. Furthermore, gene expression profiling revealed that downregulation of oxidative phosphorylation gene expression in skeletal muscle and liver leads to decreased insulin sensitivity in these tissues. Together, our findings suggest that resident alternatively activated macrophages have a beneficial role in regulating nutrient homeostasis and suggest that macrophage polarization towards the alternative state might be a useful strategy for treating type 2 diabetes.
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            Signaling pathway of MAPK/ERK in cell proliferation, differentiation, migration, senescence and apoptosis.

            Yu-Chen Sun, Wen-Zhou Liu, Tao Liu … (2015)
            The generic mitogen-activated protein kinases (MAPK) signaling pathway is shared by four distinct cascades, including the extracellular signal-related kinases (ERK1/2), Jun amino-terminal kinases (JNK1/2/3), p38-MAPK and ERK5. Mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) pathway is reported to be associated with the cell proliferation, differentiation, migration, senescence and apoptosis. The literatures were searched extensively and this review was performed to review the role of MAPK/ERK signaling pathway in cell proliferation, differentiation, migration, senescence and apoptosis.
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              Macrophage activation and polarization

              Fernando Martinez (2008)
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date (Print): 2017
                Publication date (Electronic): 31 January 2017
                Volume: 2017
                Electronic Location Identifier: 6494795
                Affiliations
                1College of Health Science & Nursing, Wuhan Polytechnic University, Wuhan, Hubei, China
                2Cardiovascular Research Institute, Case Western Reserve University, Cleveland, OH, USA
                Author notes

                Academic Editor: Monica Bullo

                Author information
                http://orcid.org/0000-0002-7922-2823
                http://orcid.org/0000-0002-3534-7480
                Article
                DOI: 10.1155/2017/6494795
                PMC ID: 5307004
                PubMed ID: 28251163
                SO-VID: 664bd974-7f01-47f7-8539-52f3aa101cd9
                Copyright © Copyright © 2017 Chang Xia et al.
                License:

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

                History
                Date received : 23 July 2016
                Date revision received : 30 December 2016
                Date accepted : 12 January 2017
                Funding
                Funded by: National Institutes of Health
                Award ID: K01 DK105108
                Award ID: P30DK072488
                Funded by: American Heart Association
                Award ID: 15SDG25700381
                Award ID: 13POST17210033
                Funded by: National Natural Science Foundation of China
                Award ID: 81670431
                Award ID: 81101247
                Funded by: Boehringer Ingelheim
                Award ID: IIS2015-10485
                Funded by: Natural Science Foundation of Zhejiang Province
                Award ID: Y2110580
                Categories
                Subject: Review Article

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