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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.

Original publication

DOI

10.1038/ni.1942

Type

Journal article

Journal

Nat Immunol

Publication Date

11/2010

Volume

11

Pages

1039 - 1046

Keywords

Animals, Cell Differentiation, Cell Line, Tumor, Female, Humans, Interleukin-10, Melanoma, Mice, Mice, Inbred C57BL, Natural Killer T-Cells, Neutrophils, Serum Amyloid A Protein