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Published on: November 17, 2023
Tissue-resident macrophages as replicative niches for intracellular pathogens
1Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Abstract:
Macrophages are considered a critical component of innate immunity against intracellular pathogens. Although macrophages have historically been viewed as monocyte-derived and terminally differentiated cells, recent progress has revealed that many tissue-resident macrophages are embryonically seeded, self-renewed, and perform homeostatic functions associated with M2-like activation programs. There is evidence that tissue-resident macrophages (TRMs) maintain their M2-like phenotype even in an infection-driven pro-inflammatory environment. In this regard, several intracellular pathogens are shown to exploit M2-like TRMs as replicative niches to evade pathogen-specific immunity. This knowledge provides a new perspective to understand the chronicity of infections and develop therapeutic strategies which can selectively target TRMs.
Insights
Tissue-resident macrophages (TRMs), often embryonically derived, can maintain an M2-like state. Some intracellular pathogens exploit these TRMs as niches, evading immunity and causing chronic infections.
Area of Science:
- Immunology
- Cell Biology
Background:
- Macrophages are key innate immune cells.
- Tissue-resident macrophages (TRMs) are increasingly recognized as self-renewing and embryonically derived.
- TRMs often exhibit M2-like activation states crucial for homeostasis.
Purpose of the Study:
- To investigate the phenotype stability of TRMs in inflammatory conditions.
- To explore the role of M2-like TRMs as potential replicative niches for intracellular pathogens.
- To understand how TRMs contribute to chronic infections.
Main Methods:
- Review of existing literature on macrophage biology and immunology.
- Analysis of studies detailing TRM origins and functions.
- Examination of pathogen-host interactions involving TRMs.
Main Results:
- TRMs can maintain their M2-like phenotype despite pro-inflammatory signals during infection.
- Certain intracellular pathogens utilize M2-like TRMs to establish replicative niches.
- This exploitation facilitates pathogen evasion of adaptive immunity.
Conclusions:
- Tissue-resident macrophages represent a critical, yet often overlooked, component in the persistence of intracellular infections.
- Understanding TRM behavior offers new avenues for therapeutic strategies targeting chronic infections.
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