Sex differences in inflammation, redox biology, mitochondria and autoimmunity

Autoimmune diseases are characterized by circulating antibodies and immune complexes directed against self-tissues that result in both systemic and organ-specific inflammation and pathology. Most autoimmune diseases occur more often in women than men. One exception is myocarditis, which is an inflam...

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Main Authors: Damian N. Di Florio, Jon Sin, Michael J. Coronado, Paldeep S. Atwal, DeLisa Fairweather
Format: Article
Language:English
Published: Elsevier 2020-04-01
Series:Redox Biology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2213231719311887
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author Damian N. Di Florio
Jon Sin
Michael J. Coronado
Paldeep S. Atwal
DeLisa Fairweather
author_facet Damian N. Di Florio
Jon Sin
Michael J. Coronado
Paldeep S. Atwal
DeLisa Fairweather
author_sort Damian N. Di Florio
collection DOAJ
description Autoimmune diseases are characterized by circulating antibodies and immune complexes directed against self-tissues that result in both systemic and organ-specific inflammation and pathology. Most autoimmune diseases occur more often in women than men. One exception is myocarditis, which is an inflammation of the myocardium that is typically caused by viral infections. Sex differences in the immune response and the role of the sex hormones estrogen and testosterone are well established based on animal models of autoimmune viral myocarditis as well as in mitochondrial function leading to reactive oxygen species production. RNA viruses like coxsackievirus B3, the primary cause of myocarditis in the US, activate the inflammasome through mitochondrial antiviral signaling protein located on the mitochondrial outer membrane. Toll-like receptor 4 and the inflammasome are the primary signaling pathways that increase inflammation during myocarditis, which is increased by testosterone. This review describes what is known about sex differences in inflammation, redox biology and mitochondrial function in the male-dominant autoimmune disease myocarditis and highlights gaps in the literature and future directions.
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spelling doaj.art-db8f9f0960c64e4b8956dbf3660151772022-12-22T00:02:22ZengElsevierRedox Biology2213-23172020-04-0131Sex differences in inflammation, redox biology, mitochondria and autoimmunityDamian N. Di Florio0Jon Sin1Michael J. Coronado2Paldeep S. Atwal3DeLisa Fairweather4Center for Clinical and Translational Science, Mayo Clinic, Jacksonville, FL, USACedars-Sinai Medical Center, Heart Institute, Los Angeles, CA, USAWhitman College, Walla Walla, WA, USAAtwal Clinic, Jacksonville, FL, USACenter for Clinical and Translational Science, Mayo Clinic, Jacksonville, FL, USA; Department of Cardiovascular Medicine, Mayo Clinic, Jacksonville, FL, USA; Department of Immunology, Mayo Clinic, Jacksonville, FL, USA; Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Corresponding author. Department of Cardiovascular Medicine, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL, USA.Autoimmune diseases are characterized by circulating antibodies and immune complexes directed against self-tissues that result in both systemic and organ-specific inflammation and pathology. Most autoimmune diseases occur more often in women than men. One exception is myocarditis, which is an inflammation of the myocardium that is typically caused by viral infections. Sex differences in the immune response and the role of the sex hormones estrogen and testosterone are well established based on animal models of autoimmune viral myocarditis as well as in mitochondrial function leading to reactive oxygen species production. RNA viruses like coxsackievirus B3, the primary cause of myocarditis in the US, activate the inflammasome through mitochondrial antiviral signaling protein located on the mitochondrial outer membrane. Toll-like receptor 4 and the inflammasome are the primary signaling pathways that increase inflammation during myocarditis, which is increased by testosterone. This review describes what is known about sex differences in inflammation, redox biology and mitochondrial function in the male-dominant autoimmune disease myocarditis and highlights gaps in the literature and future directions.http://www.sciencedirect.com/science/article/pii/S2213231719311887ROSMyocarditisMacrophageNLRP3 inflammasomeTLR4TNF
spellingShingle Damian N. Di Florio
Jon Sin
Michael J. Coronado
Paldeep S. Atwal
DeLisa Fairweather
Sex differences in inflammation, redox biology, mitochondria and autoimmunity
Redox Biology
ROS
Myocarditis
Macrophage
NLRP3 inflammasome
TLR4
TNF
title Sex differences in inflammation, redox biology, mitochondria and autoimmunity
title_full Sex differences in inflammation, redox biology, mitochondria and autoimmunity
title_fullStr Sex differences in inflammation, redox biology, mitochondria and autoimmunity
title_full_unstemmed Sex differences in inflammation, redox biology, mitochondria and autoimmunity
title_short Sex differences in inflammation, redox biology, mitochondria and autoimmunity
title_sort sex differences in inflammation redox biology mitochondria and autoimmunity
topic ROS
Myocarditis
Macrophage
NLRP3 inflammasome
TLR4
TNF
url http://www.sciencedirect.com/science/article/pii/S2213231719311887
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