Table 2.

Neutrophil subsets during pathological conditions. The table describes neutrophil subsets, including their phenotype and function, which have been identified in pathological conditions such as cancer, infection and inflammation in mice or humans. Subsets with a pro-inflammatory or anti-inflammatory phenotype are highlighted in italics and bold, respectively. IFN, interferon; IL, interleukin; i.v., intravenous; LDG, low-density granulocyte; LPS, lipopolysaccharide; MRSA, methicillin-resistant Staphylococcus aureus; PBMC, peripheral blood mononuclear cell; PMN, polymorphonuclear neutrophil; ROS, reactive oxygen species; SIRS, systemic inflammatory response syndrome; SLE, systemic lupus erythematosus; TAN, tumour-associated neutrophil; TGF, transforming growth factor; TLR, toll-like receptor.

disease model	subset	occurrence	phenotype	proposed systemic effects
murine subcutaneous tumours [10]	N1 TAN	— tumours with TGF-β inhibition	— hypersegmented nuclear morphology — high ROS production — high Fas, ICAM-1 and TNF-α expression — higher tumour cell cytotoxicity in vitro	— pro-inflammatory and anti-tumorigenic
	N2 TAN	— majority of untreated tumours	— normal, segmented nuclear morphology — suppress T-cell effector functions via arginase	— immunosuppressive and pro-tumorigenic
MRSA infection in mice [11]	PMN-I	— infected mice with mild SIRS	— normal, segmented nuclear morphology — induce classically activated macrophages — produce IL-12 and CCL3 — express TLR-2, -4, -5 and -8 and integrin α4	— protection from MRSA infection
	PMN-II	— infected mice with severe SIRS	— ring-shaped nuclear morphology — induce alternatively activated macrophages — produce IL-10 and CCL2 — express TRL-2, -4, -7 and -9 and integrin αM	— susceptibility to MRSA infection
human experimental endotoxemia [12,14]	CD16dim/CD62Lbright	— post-LPS i.v.; up to 50% of neutrophils	— immature, banded nuclear morphology — lower ROS production and interaction with opsonized bacteria — increased survival in vitro	— increased susceptibility to infection during SIRS
	CD16bright/CD62Ldim	— post-LPS i.v. or trauma; 10–15% of neutrophils	— hypersegmented nuclear morphology — increased capability to produce ROS — express integrins αM and αX and ICAM-1 — integrin αM and ROS-dependent inhibition of T-cell proliferation	— immunosuppressive; suppress T-cell proliferation
	CD16bright/CD62Lbright	— normally occurring neutrophils	— normal, segmented nuclear morphology — higher ROS production and interaction with opsonized bacteria — express integrin αM and FcγRII	— excessive tissue damage during SIRS
SLE patients [13,70]	LDG	— about 17% of PBMCs in SLE patients	— immature, banded/lobular nuclear morphology — activated phenotype: express CD66b, integrin αMβ2, type I interferons, TNF-α and IFN-γ — reduced phagocytic ability — increased capacity to form NETs — higher endothelial cell cytotoxicity in vitro	— pro-inflammatory