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      Serum IL-17, IL-23, and TGF- β Levels in Type 1 and Type 2 Diabetic Patients and Age-Matched Healthy Controls

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          Abstract

          Type 1 diabetes is recognized as an autoimmune inflammatory disease and low grade inflammation is also observed in type 2 diabetic patients. Interleukin 17 (IL-17) is a new player in inflammation. Th17 cells, as the main source of IL-17, require transforming growth factor β (TGF- β ) and interleukin 23 (IL-23). The aim of this study was to investigate serum IL-17, IL-23 and TGF- β levels in diabetic patients and controls. In this case-control study, serum levels of IL-17, IL-23, and TGF- β were measured in 24 type 1 diabetic patients and 30 healthy controls using the ELISA method. Simultaneously, the same methodology was used to compare serum concentration of these three cytokines in 38 type 2 diabetic patients and 40 healthy controls. There was no significant difference between serum levels of IL-17 and IL-23 cytokines between cases and controls. However, TGF- β was significantly lower in type 1 diabetic patients ( P < 0.001). Serum IL-17 and IL-23 levels demonstrate no association with type 1 and type 2 diabetes, but, in line with previous studies, TGF- β levels were lower in type 1 diabetic patients.

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          TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

          Marc Veldhoen, Richard J Hocking, Christopher Atkins … (2006)
          We describe de novo generation of IL-17-producing T cells from naive CD4 T cells, induced in cocultures of naive CD4 T cells and naturally occurring CD4+ CD25+ T cells (Treg) in the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha. We could not detect a role for IL-23 in the differentiation of IL-17-producing T cells but confirmed its importance for their survival and expansion. Transcription factors GATA-3 and T-bet, as well as its target Hlx, are absent in IL-17-producing T cells, and they do not express the negative regulator for TGFbeta signaling, Smad7. Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells.
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            Inflamm-aging. An evolutionary perspective on immunosenescence.

            C Franceschi, M BonaFe, S Valensin … (2000)
            In this paper we extend the "network theory of aging," and we argue that a global reduction in the capacity to cope with a variety of stressors and a concomitant progressive increase in proinflammatory status are major characteristics of the aging process. This phenomenon, which we will refer to as "inflamm-aging," is provoked by a continuous antigenic load and stress. On the basis of evolutionary studies, we also argue that the immune and the stress responses are equivalent and that antigens are nothing other than particular types of stressors. We also propose to return macrophage to its rightful place as central actor not only in the inflammatory response and immunity, but also in the stress response. The rate of reaching the threshold of proinflammatory status over which diseases/disabilities ensue and the individual capacity to cope with and adapt to stressors are assumed to be complex traits with a genetic component. Finally, we argue that the persistence of inflammatory stimuli over time represents the biologic background (first hit) favoring the susceptibility to age-related diseases/disabilities. A second hit (absence of robust gene variants and/or presence of frail gene variants) is likely necessary to develop overt organ-specific age-related diseases having an inflammatory pathogenesis, such as atherosclerosis, Alzheimer's disease, osteoporosis, and diabetes. Following this perspective, several paradoxes of healthy centenarians (increase of plasma levels of inflammatory cytokines, acute phase proteins, and coagulation factors) are illustrated and explained. In conclusion, the beneficial effects of inflammation devoted to the neutralization of dangerous/harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.
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              Inflammatory markers in population studies of aging.

              Tushar Singh, Anne Newman (2011)
              To review findings from major epidemiologic studies regarding risk factors for and consequences of elevated markers of inflammation in older adults. Most large, current epidemiologic studies of older adults have measured serum interleukin-6 (IL-6), C-reactive protein (CRP) and tumor necrosis factor alpha (TNF-alpha) and some studies also include more extensive batteries of measures including soluble receptors. There are few defined risk factors for the modest elevations in inflammatory markers seen with aging. These include visceral adiposity, lower sex steroid hormones, smoking, depression and periodontal disease. Of the markers assessed, IL-6 is most robustly associated with incident disease, disability and mortality. Though correlated with age, the etiology of elevated inflammatory markers remains incompletely defined. Inflammation, especially IL-6 may be a common cause of multiple age-related diseases or a final common pathway by which disease leads to disability and adverse outcomes in older adults. Future research targeting inflammation should examine these pathways. Copyright © 2011. Published by Elsevier B.V.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date (Print): 2014
                Publication date (Electronic): 4 June 2014
                Volume: 2014
                Electronic Location Identifier: 718946
                Affiliations
                1Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran 1417755469, Iran
                2Endocrinology and Metabolism Research Center (EMRC), Dr. Shariati Hospital, Tehran University of Medical Sciences, Tehran 1411413137, Iran
                3Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran 1417613151, Iran
                4Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran 1417613151, Iran
                5Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran 1417613151, Iran
                6Department of Public Health, Alborz University of Medical Sciences, Karaj 3139614171, Iran
                7Department of Epidemiology, Iran University of Medical Sciences, Tehran 1449614535, Iran
                8Department of Community and Preventive Medicine, School of Medicine, Tehran University of Medical Sciences, Tehran 1417613151, Iran
                9Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari 4817844718, Iran
                10Department of Pathology, Children's Medical Center Hospital, Tehran University of Medical Sciences, Tehran 1419733151, Iran
                11Farmanfarmaian Health Center, Tehran University of Medical Sciences, Tehran 1318618311, Iran
                Author notes

                Academic Editor: Robin Vos

                Article
                DOI: 10.1155/2014/718946
                PMC ID: 4065742
                PubMed ID: 24995325
                SO-VID: 054ce52a-403a-4a25-85a2-96dc35184236
                Copyright © Copyright © 2014 Azam Roohi 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 : 6 February 2014
                Date revision received : 14 May 2014
                Date accepted : 14 May 2014
                Funding
                Funded by: Deputy of Research of Tehran University of Medical Sciences
                Award ID: 88-03-87-9424
                Categories
                Subject: Research Article

                Data availability:

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