Journal
NATURE IMMUNOLOGY
Volume 11, Issue 11, Pages 1039-U92Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1942
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Funding
- Cancer Research UK [C399/A2291]
- UK Medical Research Council
- The Wellcome Trust [084923/Z/08/Z]
- Cancer Research Institute
- Ludwig Institute for Cancer Research
- Oxford National Institute for Health Research Biomedical Research Centre
- Oxford Experimental Cancer Medicine Centre
- Cancer Research UK [8466, 11331] Funding Source: researchfish
- Medical Research Council [G0501975, G1000800e, G1000800] Funding Source: researchfish
- MRC [G1000800, G0501975] Funding Source: UKRI
- Wellcome Trust [084923/Z/08/Z] Funding Source: Wellcome Trust
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Neutrophils are the main effector cells during inflammation, but they can also control excessive inflammatory responses by secreting anti-inflammatory cytokines. However, the mechanisms that modulate their plasticity remain unclear. We now show that systemic serum amyloid A 1 (SAA-1) controls the plasticity of neutrophil differentiation. SAA-1 not only induced anti-inflammatory interleukin 10 (IL-10)-secreting neutrophils but also promoted the interaction of invariant natural killer T cells (iNKT cells) with those neutrophils, a process that limited their suppressive activity by diminishing the production of IL-10 and enhancing the production of IL-12. Because SAA-1-producing melanomas promoted differentiation of IL-10-secreting neutrophils, harnessing iNKT cells could be useful therapeutically by decreasing the frequency of immunosuppressive neutrophils and restoring tumor-specific immune responses.
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