Differential roles of resident microglia and infiltrating monocytes in murine CNS autoimmunity

Macrophages can be of dual origin. Most tissue-resident macrophage compartments are generated before birth and subsequently maintain themselves independently from each other locally in healthy tissue. Under inflammatory conditions, these cells can however be complemented by macrophages derived from...

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Bibliographic Details
Published in:Seminars in Immunopathology 2015-11, Vol.37 (6), p.613-623
Main Authors: Shemer, Anat, Jung, Steffen
Format: Article
Language:English
Subjects:
Animals
Antigen Presentation - immunology
Biomedical and Life Sciences
Biomedicine
Central Nervous System - immunology
Central Nervous System - pathology
Cytokines - metabolism
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - pathology
Immunology
Inflammation - immunology
Internal Medicine
Macrophages - immunology
Mice
Microglia - immunology
Monocytes - immunology
Phagocytosis - immunology
Review
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Summary:Macrophages can be of dual origin. Most tissue-resident macrophage compartments are generated before birth and subsequently maintain themselves independently from each other locally in healthy tissue. Under inflammatory conditions, these cells can however be complemented by macrophages derived from acute monocyte infiltrates. Due to the lack of suitable experimental systems, differential functional contributions of central nervous system (CNS)-resident microglia and monocyte-derived macrophages (MoMF) to CNS inflammation, such as experimental autoimmune encephalomyelitis (EAE), the mouse model of multiple sclerosis (MS), remain poorly understood. Here, we will review recent progress in this field that suggest distinct roles of microglia and MoMF in disease induction and progression, capitalizing on novel transgenic mouse models. The latter finding could have major implications for the rationale development of therapeutic approaches to the management of brain inflammation and MS therapy.
ISSN:1863-2297
1863-2300
DOI:10.1007/s00281-015-0519-z