Cited by 274Immune cells in cancerPhagocytosis and Immune RegulationParasites and Host Interactions

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Alternative Activation Is an Innate Response to Injury That Requires CD4+ T Cells to be Sustained during Chronic Infection

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Loke, P’ng, Gallagher, Iain, Nair, Meera G, Zang, Xingxing, Brombacher, Frank, Mohrs, Markus, Allison, James P, Allen, Judith E·2007·The Journal of Immunology

DOI 10.4049/jimmunol.179.6.3926

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Abstract

Alternatively activated macrophages (AAMPhi) are found in abundance during chronic Th2 inflammatory responses to metazoan parasites. Important roles for these macrophages are being defined, particularly in the context of Th2-mediated pathology and fibrosis. However, a full understanding of the requirements for alternative activation, particularly at the innate level, is lacking. We present evidence that alternative activation by the Th2 cytokines IL-4 and IL-13 is an innate and rapid response to tissue injury that takes place even in the absence of an infectious agent. This early response does not require CD4+ Th2 cells because it occurred in RAG-deficient mice. However, class II-restricted CD4+ T cell help is essential to maintain AAMPhi in response to infection, because AAMPhi were absent in RAG-deficient and MHC class II-deficient, but not B cell-deficient mice after chronic exposure to the nematode parasite, Brugia malayi. The absence of AAMPhi was associated with increased neutrophilia and reduced eosinophilia, suggesting that AAMPhi are involved in the clearance of neutrophils as well as the recruitment of eosinophils. Consistent with this hypothesis, AAMPhi show enhanced phagocytosis of apoptotic neutrophils, but not latex beads. Our data demonstrate that alternative activation by type 2 cytokines is an innate response to injury that can occur in the absence of an adaptive response. However, analogous to classical activation by microbial pathogens, Th2 cells are required for maintenance and full activation during the ongoing response to metazoan parasites.

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Authors: Loke, P., Gallagher, I., Nair, M. G., Zang, X., Brombacher, F., Mohrs, M., Allison, J. P., & Allen, J. E.
Affiliations: University of California, San Francisco (US)
University of Edinburgh (GB)
Memorial Sloan Kettering Cancer Center (US)
University of Cape Town (ZA)
Trudeau Institute (US)
ORCID: Loke, P’ng
Gallagher, Iain
Nair, Meera G
Zang, Xingxing
Brombacher, Frank
Allison, James P
Allen, Judith E
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 2007-09
Volume: 179
Issue: 6
Pages: 3926-3936
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.179.6.3926
OpenAlex: W2152215671
Cited by: 274
References: 73
Citations by year: 2026: 2 · 2025: 6 · 2024: 10 · 2023: 1 · 2022: 4 · 2021: 9 · 2020: 5 · 2019: 5 · 2018: 18 · 2017: 15 · 2016: 19 · 2015: 21 · 2014: 22 · 2013: 26 · 2012: 31
FWCI: 6.56
Type: journal article
Language: en
Open access: green
www.research.ed.ac.uk
Licence: other-oa
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Research Explorer (The University of Manchester) (publishedVersion)
Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
Funders: Wellcome Trust
Medical Research Council
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Life Sciences › Immunology and Microbiology › Parasitology › Parasites and Host Interactions
Keywords: alternative activation, M2 macrophages, CD4+ T cells, Th2 cytokines, IL-4, IL-13, tissue damage, innate immunity, chronic infection, Brugia malayi, MHC class II, RAG-deficient mice, eosinophilia, neutrophilia, metazoan parasites
MeSH terms: Animals, Arginase, beta-N-Acetylhexosaminidases, Cell Movement, Chronic Disease, Female, Filariasis, Immunity, Active, Macrophage Activation, Male, Mice, Inbred C57BL, Neutrophils, Proteins, CD4-Positive T-Lymphocytes, Brugia malayi, Mice, Knockout, Nerve Growth Factor, Intercellular Signaling Peptides and Proteins, Lectins, Mice

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Alternative Activation Is an Innate Response to Injury That Requires CD4+ T Cells to be Sustained during Chronic Infection

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