Cited by 290Immune cells in cancerCardiac Fibrosis and RemodelingPhagocytosis and Immune Regulation

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Alternatively activated macrophages in infection and autoimmunity

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Fairweather, DeLisa, Cihakova, Daniela·2009·Journal of Autoimmunity

DOI 10.1016/j.jaut.2009.09.012PMC PMC2783278

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Abstract

Macrophages are innate immune cells that play an important role in activation of the immune response and wound healing. Pathogens that require T helper-type 2 (Th2) responses for effective clearance, such as parasitic worms, are strong inducers of alternatively activated or M2 macrophages. However, infections such as bacteria and viruses that require Th1-type responses may induce M2 as a strategy to evade the immune system. M2 are particularly efficient at scavenging self tissues following injury through receptors like the mannose receptor and scavenger receptor-A. Thus, M2 may increase autoimmune disease by presenting self tissue to T cells. M2 may also exacerbate immune complex (IC)-mediated pathology and fibrosis, a hallmark of autoimmune disease in women, due to the release of profibrotic factors such as interleukin-1beta, transforming growth factor-beta, fibronectin and matrix metalloproteinases. We have found that M2 comprise anywhere from 30% to 70% of the infiltrate during acute viral or experimental autoimmune myocarditis, and shifts in M2 populations correlate with increased IC deposition, fibrosis and chronic autoimmune pathology. Thus, women may be at an increased risk of M2-mediated autoimmunity due to estrogen's ability to increase Th2 responses.

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Authors: Fairweather, D., & Cihakova, D.
Affiliations: Johns Hopkins University (US)
Corresponding author: Fairweather, DeLisa
ORCID: Fairweather, DeLisa
Venue: Journal of Autoimmunity
Publisher: Elsevier BV
Published: 2009-11
Volume: 33
Issue: 3-4
Pages: 222-230
ISSN: 0896-8411 (ISSN-L)
DOI: 10.1016/j.jaut.2009.09.012
PMC: PMC2783278
OpenAlex: W2083198686
Cited by: 290
References: 124
Citations by year: 2026: 4 · 2025: 7 · 2024: 8 · 2023: 4 · 2022: 4 · 2021: 11 · 2020: 13 · 2019: 14 · 2018: 16 · 2017: 20 · 2016: 26 · 2015: 18 · 2014: 26 · 2013: 32 · 2012: 36
FWCI: 12.37
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Journal of Autoimmunity (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Myocarditis Foundation
National Institutes of Health
National Heart, Lung, and Blood Institute (HL 67290, R01HL087033, R01HL067290, HL 70729, R01HL070729, HL087033)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Keywords: M2 macrophages, autoimmunity, infection, Th2 immune response, Th1 response, immune evasion, fibrosis, experimental autoimmune myocarditis, viral infection, estrogen, sex differences, CD206, scavenger receptor A
MeSH terms: Animals, Autoimmune Diseases, Complement System Proteins, Female, Humans, Immunity, Cellular, Infections, Macrophage Activation, Macrophages, Male, Sex Factors, Gonadal Steroid Hormones, Cytokines, Immunity, Humoral

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