Table 1 Neutrophils treated with different stimulations display different phenotypes and regulatory function on adaptive immunity

GM-CSF, IFN-γ, IL-3

MHC-II, CD80, CD86, CD83

Undetected

Human

[10]

GM-CSF, IFN-γ

MHC-II, CD80, CD86

Undetected

Human

[11]

GM-CSF, IFN-γ, IL-4, TNF-α and M-CSF

Macrophage-like neutrophils with HLA-DR

Undetected

Human

[12]

GM-CSF, IFN-γ or combination

MHC-II, CD80, CD86 and CD83

To present peptide antigen to CD4⁺ T cells

Human

[13,14,15]

GM-CSF + IL-4 + TNF-α

HLA-DR, HLR-DQ, CD80, CD86 and CD40

Stimulate T cell proliferation

Human

[16]

Patients with acute infection

CD83

Undetected

Human

[17]

Patients with chronic inflammatory diseases

MHC-II, CD80/86

Undetected

Human

[17]

Patients with Wegener’s granulomatosis

MHC-II, CD80/86

Undetected

Human

[18, 19]

Peritoneal cavity after i.p. administration of glycogen

MHC-II

To present the lysozyme antigen to T cells

Mouse

[20, 21]

Peritoneal cavity after i.p. injection of Fusobacterium nucleatum

Undetected

Stimulate T cell proliferation

Mouse

[22]

GM-CSF

MHC-II, CD11c, CD80, CD86

To present antigens to CD4⁺ T cells

Mouse

[23]

N(IL-23)

(IL-23-stimulated)

Th17 cytokines

Undetected

Mice

[24]

N(IL-33)

(IL-33-stimulated)

Th9 cytokines

Undetected

Mice

[25]

N(LPS)

(LPS-stimulated)

TNF-α, IL-6

Undetected

Mice

[24]

GM-CSF, IFN-γ, and TNF-α in sepsis patients

CD40, CD64, CD86

Undetected

Human

[26]

Synovial fluid of patients with RA, co-cultured with autologous T cells

MHC-II, CD14, CD64, CD83

Undetected

Human

[27]

Peritoneal cavity after TG injection, co-cultured with purified CD4⁺ T cells

MHC-II, CD86

Present peptides to T cells; Stimulate T cell proliferation and cytokine production

Mice

[28, 29]

The inflamed colon in colitis mouse

MHC-II, CD86

Stimulate T cell proliferation and cytokine production

Mice

[30]

CD49d⁺CD11b⁻ N1

(from MRSA-resistant mice)

IL-12, CCL3, TLR2, TLR4, TLR5, TLR8

Th1 response

Mice

[31]

CD49d⁻CD11b⁺ N2

(from MRSA- sensitive mice)

IL-10, IL-4, CCL2, TLR2, TLR4, TLR7, TLR9

Th2 response

Mice

[31]

CD49d⁻CD11b⁻ neutrophils

(from naïve mice)

TLR2, TLR4, TLR9

no chemokines and cytokines

Mice

[31]

N1 TAN

(blockade of TGF-β in tumor microenvironment)

Immuno-activating cytokines and chemokines

anti-tumorigenic;

increasing CD8⁺ T cell activation

Mice

[32]

N2 TAN

(stimulated by TGF-β in tumor microenvironment)

Undetected

Pro-tumorigenic;

decreasing CD8⁺ T cell activation

Mice

[32]

Parasite-primed

(helminth infection)

IL-13, IL-33

macrophage activation

Mice

[33]

NCs in spleen

(infected by bacteria)

IL-12

acting as APC-like cells

Mice

[31]

CD15^interCD16^inter N_BH1

(microbes infection)

IL-21, BAFF, APRIL, CXCL12, CXCL13;

N_BH1 expresses higher CD27, CD40L, CD86, CD95 and MHC-II, than N_BH2

B cell activation

Mice

[34]

CD15^lowCD16^low N_BH2 in spleen (microbes infection)

IL-21, BAFF, APRIL, CXCL12, CXCL13; N_BH2 expresses higher CD24 than N_BH1

B cell activation

Mice

[34]