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      The Role of Tumor Necrosis Factor Alpha (TNF-α) in Autoimmune Disease and Current TNF-α Inhibitors in Therapeutics

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          Abstract

          Tumor necrosis factor alpha (TNF-α) was initially recognized as a factor that causes the necrosis of tumors, but it has been recently identified to have additional important functions as a pathological component of autoimmune diseases. TNF-α binds to two different receptors, which initiate signal transduction pathways. These pathways lead to various cellular responses, including cell survival, differentiation, and proliferation. However, the inappropriate or excessive activation of TNF-α signaling is associated with chronic inflammation and can eventually lead to the development of pathological complications such as autoimmune diseases. Understanding of the TNF-α signaling mechanism has been expanded and applied for the treatment of immune diseases, which has resulted in the development of effective therapeutic tools, including TNF-α inhibitors. Currently, clinically approved TNF-α inhibitors have shown noticeable potency in a variety of autoimmune diseases, and novel TNF-α signaling inhibitors are being clinically evaluated. In this review, we briefly introduce the impact of TNF-α signaling on autoimmune diseases and its inhibitors, which are used as therapeutic agents against autoimmune diseases.

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          Most cited references101

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          Psoriasis.

          Psoriasis is an immune-mediated, genetic disease manifesting in the skin or joints or both. A diverse team of clinicians with a range of expertise is often needed to treat the disease. Psoriasis provides many challenges including high prevalence, chronicity, disfiguration, disability, and associated comorbidity. Understanding the role of immune function in psoriasis and the interplay between the innate and adaptive immune system has helped to manage this complex disease, which affects patients far beyond the skin. In this Seminar, we highlight the clinical diversity of psoriasis and associated comorbid diseases. We describe recent developments in psoriasis epidemiology, pathogenesis, and genetics to better understand present trends in psoriasis management. Our key objective is to raise awareness of the complexity of this multifaceted disease, the potential of state-of-the-art therapeutic approaches, and the need for early diagnosis and comprehensive management of patients with psoriasis.
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            Pathogenesis and clinical features of psoriasis.

            Psoriasis, a papulosquamous skin disease, was originally thought of as a disorder primarily of epidermal keratinocytes, but is now recognised as one of the commonest immune-mediated disorders. Tumour necrosis factor alpha, dendritic cells, and T-cells all contribute substantially to its pathogenesis. In early-onset psoriasis (beginning before age 40 years), carriage of HLA-Cw6 and environmental triggers, such as beta-haemolytic streptococcal infections, are major determinants of disease expression. Moreover, at least nine chromosomal psoriasis susceptibility loci have been identified. Several clinical phenotypes of psoriasis are recognised, with chronic plaque (psoriasis vulgaris) accounting for 90% of cases. Comorbidities of psoriasis are attracting interest, and include impairment of quality of life and associated depressive illness, cardiovascular disease, and a seronegative arthritis known as psoriatic arthritis. A more complete understanding of underlying pathomechanisms is leading to new treatments, which will be discussed in the second part of this Series.
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              Necroptosis and its role in inflammation.

              Regulated cell death has essential functions in development and in adult tissue homeostasis. Necroptosis is a newly discovered pathway of regulated necrosis that requires the proteins RIPK3 and MLKL and is induced by death receptors, interferons, toll-like receptors, intracellular RNA and DNA sensors, and probably other mediators. RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Mouse-model studies have revealed important functions for necroptosis in inflammation and suggested that it could be implicated in the pathogenesis of many human inflammatory diseases. We discuss the mechanisms regulating necroptosis and its potential role in inflammation and disease.
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                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                08 March 2021
                March 2021
                : 22
                : 5
                : 2719
                Affiliations
                [1 ]Department of Medical Biotechnology, Collage of Life Science and Biotechnology, Dongguk University, Seoul 04620, Korea; sera1586@ 123456naver.com (D.-i.J.); skandkgus@ 123456dgu.ac.kr (A.-H.L.); rtrt45689@ 123456naver.com (H.-R.S.); whdgnl7576@ 123456gmail.com (J.-H.P.)
                [2 ]School of Life Science, Handong Global University, Pohang, Gyeongbuk 37554, Korea; 21900409@ 123456handong.edu
                [3 ]Department of Pharmacy, College of Pharmacy, Yonsei University, Seoul 03722, Korea
                [4 ]Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 27478, Korea; kangtbko@ 123456kku.ac.kr
                [5 ]Department of Biological Environmental Science, Collage of Life Science and Biotechnology, Dongguk University, Seoul 04620, Korea
                Author notes
                [* ]Correspondence: leesang@ 123456dgu.ac.kr (S.-R.L.); shyang@ 123456dongguk.edu (S.-H.Y.)
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0002-0786-1482
                https://orcid.org/0000-0002-4048-0411
                https://orcid.org/0000-0003-1441-9470
                https://orcid.org/0000-0002-8672-301X
                https://orcid.org/0000-0002-6880-8861
                Article
                ijms-22-02719
                10.3390/ijms22052719
                7962638
                33800290
                62d0760a-b25f-4aca-82ae-d6b109f56b05
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 31 January 2021
                : 04 March 2021
                Categories
                Review

                Molecular biology
                tnf-α,autoimmune diseases,rheumatoid arthritis,inflammatory bowel disease,psoriatic arthritis,tnf-α inhibitors

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