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

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 tr...

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Published in	International journal of molecular sciences Vol. 22; no. 5; p. 2719
Main Authors	Jang, Dan-in, Lee, A-Hyeon, Shin, Hye-Yoon, Song, Hyo-Ryeong, Park, Jong-Hwi, Kang, Tae-Bong, Lee, Sang-Ryong, Yang, Seung-Hoon
Format	Journal Article
Language	English
Published	Switzerland MDPI 08.03.2021
Subjects	Animals Autoimmune Diseases - drug therapy Autoimmune Diseases - immunology Autoimmune Diseases - pathology Chronic Disease Humans Immunologic Factors - therapeutic use Review Signal Transduction - drug effects Signal Transduction - immunology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - immunology autoimmune diseases psoriatic arthritis TNF-α rheumatoid arthritis inflammatory bowel disease TNF-α inhibitors
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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.
AbstractList	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. 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.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.
Author	Song, Hyo-Ryeong Lee, Sang-Ryong Jang, Dan-in Kang, Tae-Bong Shin, Hye-Yoon Park, Jong-Hwi Yang, Seung-Hoon Lee, A-Hyeon
AuthorAffiliation	5 Department of Biological Environmental Science, Collage of Life Science and Biotechnology, Dongguk University, Seoul 04620, Korea 2 School of Life Science, Handong Global University, Pohang, Gyeongbuk 37554, Korea; 21900409@handong.edu 4 Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 27478, Korea; kangtbko@kku.ac.kr 1 Department of Medical Biotechnology, Collage of Life Science and Biotechnology, Dongguk University, Seoul 04620, Korea; sera1586@naver.com (D.-i.J.); skandkgus@dgu.ac.kr (A.-H.L.); rtrt45689@naver.com (H.-R.S.); whdgnl7576@gmail.com (J.-H.P.) 3 Department of Pharmacy, College of Pharmacy, Yonsei University, Seoul 03722, Korea
AuthorAffiliation_xml	– name: 2 School of Life Science, Handong Global University, Pohang, Gyeongbuk 37554, Korea; 21900409@handong.edu – name: 5 Department of Biological Environmental Science, Collage of Life Science and Biotechnology, Dongguk University, Seoul 04620, Korea – name: 4 Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 27478, Korea; kangtbko@kku.ac.kr – name: 3 Department of Pharmacy, College of Pharmacy, Yonsei University, Seoul 03722, Korea – name: 1 Department of Medical Biotechnology, Collage of Life Science and Biotechnology, Dongguk University, Seoul 04620, Korea; sera1586@naver.com (D.-i.J.); skandkgus@dgu.ac.kr (A.-H.L.); rtrt45689@naver.com (H.-R.S.); whdgnl7576@gmail.com (J.-H.P.)
Author_xml	– sequence: 1 givenname: Dan-in surname: Jang fullname: Jang, Dan-in – sequence: 2 givenname: A-Hyeon orcidid: 0000-0002-0786-1482 surname: Lee fullname: Lee, A-Hyeon – sequence: 3 givenname: Hye-Yoon surname: Shin fullname: Shin, Hye-Yoon – sequence: 4 givenname: Hyo-Ryeong orcidid: 0000-0002-4048-0411 surname: Song fullname: Song, Hyo-Ryeong – sequence: 5 givenname: Jong-Hwi surname: Park fullname: Park, Jong-Hwi – sequence: 6 givenname: Tae-Bong orcidid: 0000-0003-1441-9470 surname: Kang fullname: Kang, Tae-Bong – sequence: 7 givenname: Sang-Ryong orcidid: 0000-0002-8672-301X surname: Lee fullname: Lee, Sang-Ryong – sequence: 8 givenname: Seung-Hoon orcidid: 0000-0002-6880-8861 surname: Yang fullname: Yang, Seung-Hoon
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/33800290$$D View this record in MEDLINE/PubMed
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Snippet	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...
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SubjectTerms	Animals Autoimmune Diseases - drug therapy Autoimmune Diseases - immunology Autoimmune Diseases - pathology Chronic Disease Humans Immunologic Factors - therapeutic use Review Signal Transduction - drug effects Signal Transduction - immunology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - immunology
Title	The Role of Tumor Necrosis Factor Alpha (TNF-α) in Autoimmune Disease and Current TNF-α Inhibitors in Therapeutics
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