Cross-talk between human neutrophils and innate immune cells
| Neutrophil cross-talk with . | Cross-talk outcome . | References . |
|---|---|---|
| DCs: moDCs | Reduced CD40, CD80, and CD86 expression, and decreased ability to stimulate T cell proliferation in modcs engulfing apoptotic and/or necrotic neutrophils | 1 |
| Enhancement, by fMLF-, TNFα- or LPS-activated neutrophils, of moDC maturation and ability to promote T cell proliferation and Th1 polarization, via Mac-1/DC-SIGN and/or Mac-1/CEACAM1 interactions and TNFα release | 2-3 | |
| Enhancement, by apoptotic and/or live neutrophils, of moDC maturation and ability to promote T cell proliferation, via CD18-mediated contact dependent mechanisms and release of soluble factors | 4 | |
| Inhibition, by non-infected apoptotic neutrophils, of M tuberculosis-induced moDC maturation and ability to induce lymphocyte proliferation. Enhancement of moDC ability to drive lymphocyte proliferation by M tuberculosis-induced apoptotic neutrophils | 5 | |
| Promotion of CD4+FOXP3+ Treg differentiation by moDCs treated with neutrophil-derived elastase | 6-7 | |
| Inhibition, by neutrophil-derived EVs, of moDC maturation and capacity to induce T cell proliferation | 8 | |
| Enhancement, by BCG-infected neutrophils, of moDC maturation and ability to recall reactivity of T cells isolated from vaccinated donors, via cell-contact dependent mechanisms | 9 | |
| Modulation of DC functions by neutrophil-derived alarmins (defensins, cathelicidin, lactoferrin and high-mobility group box-1 protein) | Reviewed in Dumitru et al10 | |
| moDC internalization and cross-presentation of antigens previously processed by neutrophils | 11 | |
| Inhibition of moDC maturation and cytokine production by neutrophil-derived myeloperoxidase | 12 | |
| pDCs | Enhancement of pDC-derived IFNα by NETs released by SLE neutrophils containing self-DNA in complex with antimicrobial peptides | 13-14 |
| Enhancement of pDC-derived IFNα by NETs containing DNA complexed with secretory leukocyte protease inhibitor and neutrophil elastase or cathepsin G | 15-16 | |
| slanDCs | Enhancement, by neutrophils, of slanDC-derived IL-12p70, via CD18/ICAM-1 interactions | 17 |
| Enhancement of neutrophil and slanDC survival by reciprocal interactions occurring through contact-dependent mechanisms | 18 | |
| Macrophages | Inhibition of proinflammatory cytokine production in macrophages engulfing apoptotic neutrophils | Reviewed in Bowers et al19 |
| Inhibition of macrophage activation, cytokine production and phagocytosis by neutrophil-derived EVs | 20-21 | |
| Enhancement of macrophage antimicrobial activity by the uptake of antimicrobial peptides from neutrophils | Reviewed in Rieber et al22 | |
| Enhancement of macrophage phagocytosis and reactive oxygen species (ROS) production by neutrophil-derived primary granule proteins | 23-24 | |
| Enhancement of macrophage-derived cytokines by M tuberculosis-induced NETs | 25 | |
| Activation of NLRP3 inflammasome and induction of IL-1β and IL-18 release in macrophages by NETs from LPS-activated neutrophils or resting LDGs from SLE patients | 26 | |
| Enhancement, by PMA-induced NETs, of cytokine production in LPS-stimulated macrophages. Clearance of PMA-induced NETs by resting macrophages | 27 | |
| NK cells | Modulation, by NK cells, of neutrophil survival, activation and HB-EGF release, via GM-CSF, IFNγ and TNFα release as well as contact-dependent mechanisms | 28-29 |
| Enhancement, by neutrophils, of NK-derived IFNγ, via ICAM-3 and CD11d/CD18 interactions | 17,30 | |
| Modulation of NK cell functions by neutrophil-derived molecules, such as arginase-1, serine proteases, defensins and ROS | Reviewed in Tsuda et al31 | |
| Impairment of NK cell maturation and functions in neutropenic patients, additionally supported by in vivo experimental models | 32 | |
| Induction, by NK cells, of caspase-dependent neutrophil apoptosis, via NKp46- and Fas-dependent mechanisms | 33 | |
| Enhancement, by NK cells, of neutrophil antifungal activity. Inhibition of NK cell activation by neutrophils in the presence of Candida albicans | 34 | |
| Inhibition of pro-inflammatory, and enhancement of anti-inflammatory, cytokine production in NK cells, by neutrophil–derived EVs | 35 | |
| Induction, by NK cells, of apoptosis in galactosaminogalactan (GG)-treated neutrophils, via NKG2D mediated interactions | 36 | |
| ILCs | Enhancement of neutrophil B-cell helper functions by splenic ILCs, via GM-CSF | 37 |
| Neutrophil cross-talk with . | Cross-talk outcome . | References . |
|---|---|---|
| DCs: moDCs | Reduced CD40, CD80, and CD86 expression, and decreased ability to stimulate T cell proliferation in modcs engulfing apoptotic and/or necrotic neutrophils | 1 |
| Enhancement, by fMLF-, TNFα- or LPS-activated neutrophils, of moDC maturation and ability to promote T cell proliferation and Th1 polarization, via Mac-1/DC-SIGN and/or Mac-1/CEACAM1 interactions and TNFα release | 2-3 | |
| Enhancement, by apoptotic and/or live neutrophils, of moDC maturation and ability to promote T cell proliferation, via CD18-mediated contact dependent mechanisms and release of soluble factors | 4 | |
| Inhibition, by non-infected apoptotic neutrophils, of M tuberculosis-induced moDC maturation and ability to induce lymphocyte proliferation. Enhancement of moDC ability to drive lymphocyte proliferation by M tuberculosis-induced apoptotic neutrophils | 5 | |
| Promotion of CD4+FOXP3+ Treg differentiation by moDCs treated with neutrophil-derived elastase | 6-7 | |
| Inhibition, by neutrophil-derived EVs, of moDC maturation and capacity to induce T cell proliferation | 8 | |
| Enhancement, by BCG-infected neutrophils, of moDC maturation and ability to recall reactivity of T cells isolated from vaccinated donors, via cell-contact dependent mechanisms | 9 | |
| Modulation of DC functions by neutrophil-derived alarmins (defensins, cathelicidin, lactoferrin and high-mobility group box-1 protein) | Reviewed in Dumitru et al10 | |
| moDC internalization and cross-presentation of antigens previously processed by neutrophils | 11 | |
| Inhibition of moDC maturation and cytokine production by neutrophil-derived myeloperoxidase | 12 | |
| pDCs | Enhancement of pDC-derived IFNα by NETs released by SLE neutrophils containing self-DNA in complex with antimicrobial peptides | 13-14 |
| Enhancement of pDC-derived IFNα by NETs containing DNA complexed with secretory leukocyte protease inhibitor and neutrophil elastase or cathepsin G | 15-16 | |
| slanDCs | Enhancement, by neutrophils, of slanDC-derived IL-12p70, via CD18/ICAM-1 interactions | 17 |
| Enhancement of neutrophil and slanDC survival by reciprocal interactions occurring through contact-dependent mechanisms | 18 | |
| Macrophages | Inhibition of proinflammatory cytokine production in macrophages engulfing apoptotic neutrophils | Reviewed in Bowers et al19 |
| Inhibition of macrophage activation, cytokine production and phagocytosis by neutrophil-derived EVs | 20-21 | |
| Enhancement of macrophage antimicrobial activity by the uptake of antimicrobial peptides from neutrophils | Reviewed in Rieber et al22 | |
| Enhancement of macrophage phagocytosis and reactive oxygen species (ROS) production by neutrophil-derived primary granule proteins | 23-24 | |
| Enhancement of macrophage-derived cytokines by M tuberculosis-induced NETs | 25 | |
| Activation of NLRP3 inflammasome and induction of IL-1β and IL-18 release in macrophages by NETs from LPS-activated neutrophils or resting LDGs from SLE patients | 26 | |
| Enhancement, by PMA-induced NETs, of cytokine production in LPS-stimulated macrophages. Clearance of PMA-induced NETs by resting macrophages | 27 | |
| NK cells | Modulation, by NK cells, of neutrophil survival, activation and HB-EGF release, via GM-CSF, IFNγ and TNFα release as well as contact-dependent mechanisms | 28-29 |
| Enhancement, by neutrophils, of NK-derived IFNγ, via ICAM-3 and CD11d/CD18 interactions | 17,30 | |
| Modulation of NK cell functions by neutrophil-derived molecules, such as arginase-1, serine proteases, defensins and ROS | Reviewed in Tsuda et al31 | |
| Impairment of NK cell maturation and functions in neutropenic patients, additionally supported by in vivo experimental models | 32 | |
| Induction, by NK cells, of caspase-dependent neutrophil apoptosis, via NKp46- and Fas-dependent mechanisms | 33 | |
| Enhancement, by NK cells, of neutrophil antifungal activity. Inhibition of NK cell activation by neutrophils in the presence of Candida albicans | 34 | |
| Inhibition of pro-inflammatory, and enhancement of anti-inflammatory, cytokine production in NK cells, by neutrophil–derived EVs | 35 | |
| Induction, by NK cells, of apoptosis in galactosaminogalactan (GG)-treated neutrophils, via NKG2D mediated interactions | 36 | |
| ILCs | Enhancement of neutrophil B-cell helper functions by splenic ILCs, via GM-CSF | 37 |
References to Table 1 are listed in the supplemental Materials.