The Role of IL-17 and Th17 Lymphocytes in Autoimmune Diseases

Tabarkiewicz, Jacek; Pogoda, Katarzyna; Karczmarczyk, Agnieszka; Pożarowski, Piotr; Giannopoulos, Krzysztof

doi:10.1007/s00005-015-0344-z

Cited by 198 publications

(145 citation statements)

References 183 publications

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“…For example, there is an expansion of the Th17 subset. These cells produce and release IL-17; in more detail, they are able to produce only IL-17A and IL-17F, 2 of the 6 IL-17 isoforms (A-F) currently known [23] . There is also impairment in the differentiation of T CD4+ cells in Th1 and Th2 pools [19] .…”

Section: Autoimmunity In the Elderlymentioning

confidence: 99%

Autoimmunity in the Elderly: Insights from Basic Science and Clinics - A Mini-Review

Watad¹,

et al. 2017

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Advancements in the field of biomedicine, including the control of infectious diseases through antibiotics and vaccination practices and the prevention of chronic disorders, have led to reduced mortality, increased life expectancy and, as such, growth of the older population. Ageing is accompanied by profound morphological and physiological alterations. In particular, the immune system undergoes a complex series of remodeling/restructuring events, involving almost all compartments - both the innate and the adaptive system. This process is termed immunosenescence or immune dysregulation and, basically, includes 3 events: a reduction in immune response, an increase in the inflammatory and oxidation background (inflammaging and oxi-inflammaging), and a production of autoantibodies. While there is an increase in autoimmunity in the elderly, this does not always translate into an increase in autoimmune diseases, which represent an important cause of morbidity and mortality and affect 5-10% of the world population. Each disease involves a specific age group. Generally speaking, most autoimmune diseases have a decreased peak age of onset, except for very few diseases such as giant cell arteritis and primary biliary cirrhosis, which are more prevalent among the elderly, or inflammatory bowel disease, which has 2 peaks of onset, the first one in young subjects and the other in those older than 60 years. Autoimmune disorders in the elderly have unique clinical presentations, and insidious and atypical symptoms may constitute a challenge for the physician. They are generally milder than in adults and can be controlled by a proper therapeutic treatment. However, despite advancements both in basic and clinical sciences, further studies and investigations are warranted and should be carried out in order to dissect the molecular framework induced by ageing.

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Section: Autoimmunity In the Elderlymentioning

confidence: 99%

Autoimmunity in the Elderly: Insights from Basic Science and Clinics - A Mini-Review

Watad¹,

et al. 2017

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“…Th17 cells are key effector T cells involved in the development and pathogenesis of a variety of ADs including SLE and rheumatoid arthritis (RA) (Han et al, 2015; Korn et al, 2009; Perl, 2016; Singh et al, 2014; Tabarkiewicz et al, 2015). To assess the effects of MDA-protein adducts on adaptive immune responses, splenocytes isolated from PCE-treated and control mice were labeled with CFSE and cultured with or without MDA-MSA.…”

Section: Resultsmentioning

confidence: 99%

“…Th17 cells, which produce IL-17, IL-21 and IL-22, play a critical role in the development and pathogenesis of a variety of ADs, including SLE, RA and multiple sclerosis (Han et al, 2015; Korn et al, 2009; Perl, 2016; Singh et al, 2014; Tabarkiewicz et al, 2015). Recent studies suggest the potential role of LDA-modified endogenous proteins in the ADs (Kurien and Scofield, 2008; Grimsrud et al, 2008; Wang et al, 2010, 2016; Ben Mansour et al, 2010; Otaki et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Autoimmune potential of perchloroethylene: Role of lipid-derived aldehydes

Wang

Ansari

et al. 2017

Toxicology and Applied Pharmacology

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Tetrachloroethene (perchloroethylene, PCE), an ubiquitous environmental contaminant, has been implicated in inducing autoimmunity/autoimmune diseases (ADs), including systemic lupus erythematosus (SLE) and scleroderma in humans. However, experimental evidence suggesting the potential of PCE in mediating autoimmunity is lacking. This study was, therefore, undertaken to explore PCE’s potential in inducing/exacerbating an autoimmune response. Six-week old female MRL+/+ mice, in groups of 6 each, were treated with PCE (0.5 mg/ml) via drinking water for 12, 18 and 24 weeks and markers of autoimmunity and oxidative stress were evaluated. PCE exposure led to significant increases in serum anti-nuclear antibodies (ANA), anti-dsDNA and anti-scleroderma-70 (anti-Scl-70) antibodies at 18 weeks and, to a greater extent at 24 weeks, suggesting that PCE exposure exacerbated autoimmunity in our animal model. The increases in autoantibodies were associated with time-dependent increases in malondialdehyde (MDA)-protein adducts and their antibodies, as well as significantly decreased levels of antioxidants GSH and SOD. The splenocytes isolated from mice treated with PCE for 18 and 24 weeks showed greater Th17 cell proliferation and increased release of IL-17 in culture supernatants following stimulation with MDA-mouse serum albumin adducts, suggesting that MDA-modified proteins may act as an immunologic trigger by activating Th17 cells and contribute to PCE-mediated autoimmunity. Our studies thus provide an experimental evidence that PCE induces/exacerbates an autoimmune response and lipid-derived aldehydes (such as MDA) contribute to this response.

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“…Shao et al (2009) believed that Th17 and Treg cells have an obvious effect on the maintenance of inflammatory and immune homeostasis. Reducing Treg cells and increasing Th17 cells can lead to the incidence of renal allograft rejection, lupus nephropathy, immunoglobulin A(IgA) nephropathy, hyperplasia of glomerular nephritis, nephritis, acute coronary comprehensive syndrome, allergic purpura, and other diseases (Turner et al, 2010;Yu et al, 2013;ZambranoZaragoza et al, 2014;Feng et al, 2015;Tabarkiewicz et al, 2015) .…”

Section: Discussionmentioning

confidence: 99%

Th17/Treg cell expression in children with primary nephritic syndrome and the effects of ox-LDL on Th17/Treg cells

Wei

Zhao

et al. 2016

Genet. Mol. Res.

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ABSTRACT.To investigate the role of T-helper cells/Treg (Th17/ Treg) and morbidity factors related to primary nephritic syndrome (PNS) in children, as well as the influence of ox-low density lipoprotein (ox-LDL) on Th17/Treg expression in children with PNS. To clarify the pathogenesis of PNS in children, 50 children with PNS treated in our hospital were enrolled in the study group. Additionally, 20 healthy children who came to our hospital for physical examination during the same period were enrolled in the control group. Th17 and Treg cells in children belonging to the two groups were detected by flow cytometry; the numbers of Th17/Treg cells in peripheral blood mononuclear cells at different concentrations of ox-LDL were detected simultaneously. Ox-LDL can affect the number of Th17/Treg cells in peripheral blood mononuclear cells, and both cell types decreased with increasing concentration of ox-LDL, with the numbers being significantly lower in the control group. However, the decrease in the number of Th17 cells was statistically insignificant (P > 0.05), whereas the decrease in Treg cells was more obvious and statistically significant (P < 0.05). The effect of ox-LDL the number of Treg cells was stronger than that on Th17 cells. We concluded that the imbalance of Th17/Treg cells influenced by high and low ox-LDL concentrations in children with PNS might be the immunological basis of the disease.

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The Role of IL-17 and Th17 Lymphocytes in Autoimmune Diseases

Cited by 198 publications

References 183 publications

Autoimmunity in the Elderly: Insights from Basic Science and Clinics - A Mini-Review

Autoimmunity in the Elderly: Insights from Basic Science and Clinics - A Mini-Review

Autoimmune potential of perchloroethylene: Role of lipid-derived aldehydes

Th17/Treg cell expression in children with primary nephritic syndrome and the effects of ox-LDL on Th17/Treg cells

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