Cross-talk between human neutrophils and adaptive immune cells
| Neutrophil cross-talk with . | Cross-talk outcome . | References . |
|---|---|---|
| T cells: CD4+ and/ or CD8+ T cells | Induction, by antigen-pulsed neutrophils, of lymphocyte proliferation in a non-MHC-restricted fashion | 1 |
| Induction of antigen specific T cell activation by neutrophil precursors that have acquired DC-like properties after treatment with GM-CSF, IL-4 and TNFα | 2 | |
| MHC class II-restricted antigen presentation to T cells by GM-CSF plus IFNγ-treated neutrophils | 3-4 | |
| Enhancement of T cell proliferation by neutrophils from patients with Staphylococcus aureus infections | 5 | |
| Cross-presentation, by neutrophils, of soluble antigens to CD8+T cells | 6 | |
| Neutrophil and T cell reciprocal modulation of lifespan and function, via cytokine release and/or cell-contact dependent mechanisms | Reviewed in Kolaczkowska and Kubes7 | |
| Enhancement of neutrophil survival and activation by anti-CD3-activated CD4+T and, more potently, CD8+T cells, via TNFα, IFNγ and GM-CSF release | 8 | |
| Recruitment of Th1 and Th17, but not Th2, cells by neutrophils. Enhancement of neutrophil recruitment, survival and activation by Th17 cells, mostly via CXCL8/IL-8 and GM-CSF release, respectively | 9 | |
| Reduction of viability, activation and proliferation of CD4+T cells by unstimulated neutrophils | 10 | |
| Inhibition of T cell activation, proliferation and function by activated neutrophils, via release of arginase-1, production of ROS and/or cell-contact dependent mechanisms | 11-13 | |
| Inhibition of CD4+T cell activation and proliferation by splenic neutrophils | 14 | |
| Inhibition of T cell activation and proliferation by CD11cbright/CD62Ldim/CD11bbright/CD16bright neutrophils isolated from individuals injected with endotoxin, via Mac-1-, ROS- and/or PDL-1 (B7-H1)- dependent mechanisms | 15-16 | |
| Inhibition of T cell activation and proliferation by activated mature neutrophils or granulocytic myeloid-derived suppressor cells (G-MDSCs) from cancer patients, mainly via arginase-1 and ROS overproduction | Reviewed in Wang et al17 | |
| Priming of T cell responses to specific antigens by NETs | 18 | |
| Tregs | Recruitment of neutrophils by Tregs, via CXCL8/IL-8 release | 19 |
| Promotion of CD4+FOXP3+ Treg differentiation by moDCs treated with neutrophil-derived elastase | 20-21 | |
| γδ T cells | Killing of LPS-treated neutrophils by γδ T cells, via contact dependent mechanisms mediated by surface heat shock protein-72 | 22 |
| Enhancement of neutrophil migration, phagocytosis and α-defensin release by zoledronic acid-activated γδ T cells, via release of soluble factors | 23 | |
| Enhancement of neutrophil survival and activation by phosphoantigen activated-γδ T cells. Activation of γδ T cells by neutrophils harboring phagocytosed bacteria | 24 | |
| Suppression of spontaneous and phosphoantigen-induced activation in γδ T cells by neutrophils, via ROS production | 25 | |
| Inhibition of zoledronate-mediated Vγ9Vδ2 T cell activation by neutrophils, via hydrogen peroxide, serine proteases and arginase-1 release | 26 | |
| Enhancement of the migration, survival and proliferation of tumor infiltrated G-MDSCs by activated γδ T isolated from tumor tissues | 27 | |
| iNKT cells | Inhibition of iNKT-derived IFNγ and iNKT cytotoxicity by neutrophils, via contact dependent mechanisms | 28 |
| B cells | Enhancement of B cell survival and proliferation by G-CSF-or antineutrophil cytoplasmic antibody (ANCA)-stimulated neutrophils, via BAFF production | 29-30 |
| Enhancement of plasma cell survival by neutrophils, via APRIL secretion | 31 | |
| Induction of immunoglobulin (Ig) class switching, somatic hypermutation and antibody production in MZ B cells by splenic neutrophils, via BAFF, APRIL and IL-21 production | 14 |
| Neutrophil cross-talk with . | Cross-talk outcome . | References . |
|---|---|---|
| T cells: CD4+ and/ or CD8+ T cells | Induction, by antigen-pulsed neutrophils, of lymphocyte proliferation in a non-MHC-restricted fashion | 1 |
| Induction of antigen specific T cell activation by neutrophil precursors that have acquired DC-like properties after treatment with GM-CSF, IL-4 and TNFα | 2 | |
| MHC class II-restricted antigen presentation to T cells by GM-CSF plus IFNγ-treated neutrophils | 3-4 | |
| Enhancement of T cell proliferation by neutrophils from patients with Staphylococcus aureus infections | 5 | |
| Cross-presentation, by neutrophils, of soluble antigens to CD8+T cells | 6 | |
| Neutrophil and T cell reciprocal modulation of lifespan and function, via cytokine release and/or cell-contact dependent mechanisms | Reviewed in Kolaczkowska and Kubes7 | |
| Enhancement of neutrophil survival and activation by anti-CD3-activated CD4+T and, more potently, CD8+T cells, via TNFα, IFNγ and GM-CSF release | 8 | |
| Recruitment of Th1 and Th17, but not Th2, cells by neutrophils. Enhancement of neutrophil recruitment, survival and activation by Th17 cells, mostly via CXCL8/IL-8 and GM-CSF release, respectively | 9 | |
| Reduction of viability, activation and proliferation of CD4+T cells by unstimulated neutrophils | 10 | |
| Inhibition of T cell activation, proliferation and function by activated neutrophils, via release of arginase-1, production of ROS and/or cell-contact dependent mechanisms | 11-13 | |
| Inhibition of CD4+T cell activation and proliferation by splenic neutrophils | 14 | |
| Inhibition of T cell activation and proliferation by CD11cbright/CD62Ldim/CD11bbright/CD16bright neutrophils isolated from individuals injected with endotoxin, via Mac-1-, ROS- and/or PDL-1 (B7-H1)- dependent mechanisms | 15-16 | |
| Inhibition of T cell activation and proliferation by activated mature neutrophils or granulocytic myeloid-derived suppressor cells (G-MDSCs) from cancer patients, mainly via arginase-1 and ROS overproduction | Reviewed in Wang et al17 | |
| Priming of T cell responses to specific antigens by NETs | 18 | |
| Tregs | Recruitment of neutrophils by Tregs, via CXCL8/IL-8 release | 19 |
| Promotion of CD4+FOXP3+ Treg differentiation by moDCs treated with neutrophil-derived elastase | 20-21 | |
| γδ T cells | Killing of LPS-treated neutrophils by γδ T cells, via contact dependent mechanisms mediated by surface heat shock protein-72 | 22 |
| Enhancement of neutrophil migration, phagocytosis and α-defensin release by zoledronic acid-activated γδ T cells, via release of soluble factors | 23 | |
| Enhancement of neutrophil survival and activation by phosphoantigen activated-γδ T cells. Activation of γδ T cells by neutrophils harboring phagocytosed bacteria | 24 | |
| Suppression of spontaneous and phosphoantigen-induced activation in γδ T cells by neutrophils, via ROS production | 25 | |
| Inhibition of zoledronate-mediated Vγ9Vδ2 T cell activation by neutrophils, via hydrogen peroxide, serine proteases and arginase-1 release | 26 | |
| Enhancement of the migration, survival and proliferation of tumor infiltrated G-MDSCs by activated γδ T isolated from tumor tissues | 27 | |
| iNKT cells | Inhibition of iNKT-derived IFNγ and iNKT cytotoxicity by neutrophils, via contact dependent mechanisms | 28 |
| B cells | Enhancement of B cell survival and proliferation by G-CSF-or antineutrophil cytoplasmic antibody (ANCA)-stimulated neutrophils, via BAFF production | 29-30 |
| Enhancement of plasma cell survival by neutrophils, via APRIL secretion | 31 | |
| Induction of immunoglobulin (Ig) class switching, somatic hypermutation and antibody production in MZ B cells by splenic neutrophils, via BAFF, APRIL and IL-21 production | 14 |
iNKT, invariant NKT cells.
References to Table 2 are listed in the supplemental Materials.