Page 167 - Veterinary Immunology, 10th Edition

Macrophages are divided into two subsets based on their activation
VetBooks.ir states and functions. M1 cells promote host defense through

inflammation. M2 cells suppress inflammation and promote tissue
repair. This polarization is not necessarily permanent. Macrophages

can change their phenotype under the influence of other cytokines
and microbial products. M1 and M2 cells should perhaps be
considered a spectrum of phenotypes rather than distinct
subpopulations.

M1 cells generate large amounts of RNS, and their function is
enhanced by exposure to granulocyte-macrophage colony
stimulating factor (GM-CSF), type I interferons, and IFN-γ as well
as microbial pathogens and their products. The sustained

production of RNS permits M1 macrophages to kill bacteria, fungi,
protozoa, and some helminths, but at the cost of some tissue
damage.
The second macrophage subset, called M2 cells, is generated by

exposure to macrophage colony stimulating factor (M-CSF) and IL-
4. M2 cells do not produce NO but instead convert arginine to
ornithine using the enzyme arginase. These two macrophage
populations play different roles in defending the body. M1 cells

defend against microbial invaders and produce proinflammatory
cytokines. M2 cells have opposite effects: they reduce inflammation
and produce cytokines that suppress immune responses. M2 cells
thus promote blood vessel formation, tissue remodeling, and tissue

repair. M1 cells are produced early in the inflammatory process
when inflammation is required. M2 cells, on the other hand, tend to
appear late in the process when healing is required. M1 and M2
cells are attracted by different chemokine mixtures.

A third subset of macrophages, regulatory macrophages, are
generated by exposure to the cytokine, interleukin-10 (IL-10). They
have potent antiinflammatory activity and are discussed in Chapter
20.

Activation

Although macrophages are competent phagocytes, their activities
are greatly enhanced by several activating pathways. Neutrophil
granule proteins enhance monocyte adherence to vascular

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