Table 2 Phenotype of monocyte-derived tissue macrophages in selected pathologies

Inflammation/infection

Ly6C+, FcgammaRIII+. Distinct precursors give rise to iNOS+, CD209a-, MHC- microbicidal macrophages and CD209+ MHCII+ monocyte-derived DC

GM-CSF induces differentiation of distinct GM and MDC progenitors

[111]

Th1-mediated granuloma formation (e.g. Tuberculosis)

Classic M1 activation (IFN gamma), epithelioid transformation (adhesion molecules), foam cells (lipid storage), Langhans giant cells (DC-STAMP fusion)

Cell necrosis, caseation, cavitation (metalloproteinases) and fibrosis

iNOS+ PMN-recruited and metabolic switch

[116, 117]

TH2 cell-mediated granuloma formation (e.g. Schistosome eggs)

Alternative M2 activation (IL-4/13), multinucleated giant cells (CD36-mediated) and fibrosis (TGF beta)

TGM2+, arginase, upregulation of CR3 function. Metalloproteinases, metabolic switch, eosinophils and mast cells

[118, 119]

Bleomycin-induced fibrosis

Atypical fibrogenic monocytes (SatM) arise from Ceacam1+ SR-A+ Ly6C- F4/80- Mac1+ precursors

Arise from Ly6C- Fc ϵ R1 granulocytic/macrophage progenitors, licensed by C/EBPbeta

[18]

Atherosclerosis

Monocyte and platelets adhere to altered endothelium, foamy macrophages (cholesterol and apolipoproteins) and migrating smooth muscle cells Macrophages promote plaque rupture, coagulation and embolism

CSF-1 upregulates SR-A and metalloproteinases

[120]

Cancer:

Tumour-associated macrophages (TAMs)

Tumour attracts monocytes, macrophages contribute to tumour growth and angiogenesis

CSF-1. F4/80 promotes immune tolerance

[3]

Myeloid-derived suppressor cells (MDSC)

Abnormal differentiation of monocytes and granulocytes. Immunosuppression

Essential metabolite consumption. Reactive oxygen and nitrogen, display inhibitory surface molecules to alter T-cell trafficking and viability

[24]

Metastasis-associated macrophages (MAM)

Macrophages promote intra- and extravasation and survival of the tumour cells. Monocytes are Ly6C+ F4/80+ CD11b + CCR2+ Flt-1hi Tie2hi VEGF+

Flt-1 signalling, CSF-1 pathway, FAK(p), MAPK(p)

[121]