Journal
JOURNAL OF IMMUNOLOGY
Volume 164, Issue 9, Pages 4783-4789Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.164.9.4783
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Funding
- NCI NIH HHS [R01-CA81125-01] Funding Source: Medline
- NHLBI NIH HHS [R01-HL62052, R01-HL61721] Funding Source: Medline
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IL-17 is a novel, CD4(+) T cell-restricted cytokine. In vivo, it stimulates hematopoiesis and causes neutrophilia consisting of mature granulocytes. In this study, we show that IL-17-mediated granulopoiesis requires G-CSF release and the presence or induction of the transmembrane form of stem cell factor (SCF) for optimal granulopoiesis. However, IL-17 also protects mice from G-CSF neutralization-induced neutropenia, G-CSF neutralization completely reversed IL-17-induced BM progenitor expansion, whereas splenic CFU-GM/CFU-granulocyte-erythrocyte-megakaryocyte-monocyte was only reduced by 50% in both Sl/Sld and littermate control mice. Thus, there remained a significant SCF/G-CSF-independent effect of IL-17 on splenic granulopoiesis, resulting in a preservation of mature circulating granulocytes. IL-17 is a cytokine that potentially interconnects lymphocytic and myeloid host defense and may have potential for therapeutic development.
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