Subset |
M1 classical |
M2a alternative |
M2b type II |
M2c deactivated |
Function/phenotype |
|
|
|
|
Stimulation/Differentiation |
LPS, IFNγ, GM-CSF |
L-4 / IL-13 |
IC, LPS, IL-1β |
IL-10, TGFβ, Glucocorticoids |
Cytokine expression |
TNFα,IL-1b,IL-6,IL-12,IL-18, IL-23, IL-10low |
IL-12low,IL-23low, TGFβ, IL-10high, IL-1Ra, sIL-1R, II decoy |
IL-10high,IL-12low, IL-23low, TNFα, IL-1b, IL-6 |
IL-10high,IL-12low, IL-23low, TGFβ |
Chemokine expression |
CCL2,3,4,5,11,17 & 22 CXCL1,2,3,5,8,9,10, 11 & 16 |
CCL-17, CCL18, CCL-22, CCL-24 |
CCL-1 |
CCL-16, CCL-18 CXCL13 |
Scavenger Receptor expression |
- |
SR, MR |
- |
MR, CD163 |
Signalling |
STAT-1, STAT-4, SOCS-3 |
STAT-3 |
- |
STAT-6 |
Tryptophan metabolism |
iNOS |
Arg+ |
iNOS |
Arg+ |
Function |
Anti-microbial Pro-inflammatory Tissue-damage Th1CMI response Anti-Tumoural |
Anti-parasitic Allergic response Tissue repair Th2 response |
Anti-parasitic Allergic response Humoral immun. Th2 response |
Anti-inflammatory Immunoregulation Scavenger Tissue-repair Tumour promotion |
|
Table 1: Macrophage functional phenotypes of defined subsets: M1 classical and M2 alternatively activated phenotypes are characterised according to polarising stimulation/differentiation signals, cytokine and chemokine expression, scavenger/phagocytic receptors, tryptophan metabolism and intracellular signalling molecules. In general iNOS Mφs are M1 and Arg+ Mφs are M2; defining subsets as pro-inflammatory and driving CMI/anti-tumoral responses or anti-inflammato8/ry and driving humoral/regulatory and pro-tumoral responses, respectively. Although M1 classical and M2 alternatively activated subsets are generally acknowledged, no firm evidence exists for the existence of the M2- variants, M2a, M2b and M2c. Note the expression of iNOS by M2b subset; a characteristic more typical of M1 Mφs. It is possible that these additional subsets may represent intermediates between M1 and M2 Mφs. This table has been adapted from [8,10,18,46,80]. |