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Regulation and consequences of monocytosis
Author(s) -
Dutta Partha,
Nahrendorf Matthias
Publication year - 2014
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12219
Subject(s) - monocytosis , inflammation , immunology , biology , haematopoiesis , macrophage , monocyte , bone marrow , chemokine , innate immune system , immune system , microbiology and biotechnology , stem cell , biochemistry , in vitro
Summary Monocytes are part of the vertebrate innate immune system. Blood monocytes are produced by bone marrow and splenic progenitors that derive from hematopoietic stem cells ( HSC s). In cardiovascular disease, such as atherosclerosis and myocardial infarction, HSC s proliferate at higher levels that in turn increase production of hematopoietic cells, including monocytes. Once produced in hematopoietic niches, monocytes intravasate blood vessels, circulate, and migrate to sites of inflammation. Monocyte recruitment to atherosclerotic plaque and the ischemic heart depends on various chemokines, such as CCL 2, CX 3 CL 1, and CCL 5. Once in tissue, monocytes can differentiate into macrophages and dendritic cells. Macrophages are end effector cells that regulate the steady state and tissue healing, but they can also promote disease. At sites of inflammation, monocytes and macrophages produce inflammatory cytokines, which can exacerbate disease progression. Macrophages can also phagocytose tissue debris and produce pro‐healing cytokines. Additionally, macrophages are antigen‐presenting cells and can prime T cells. The tissue environment, including cytokines and types of inflammation, instructs macrophage specialization. Understanding monocytosis and its consequences in disease will reveal new therapeutic opportunities without compromising steady state functions.