Journal
JOURNAL OF IMMUNOLOGY
Volume 174, Issue 11, Pages 7050-7056Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.11.7050
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Funding
- NCI NIH HHS [R01CA86412] Funding Source: Medline
- NIAID NIH HHS [R29AI43184, R01AI52381] Funding Source: Medline
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Intravenous and orally administered beta-glucans promote tumor regression and survival by priming granulocyte and macrophage C receptor 3 (CR3, iC3bR and CD11b/CD18) to trigger the cytotoxicity of tumor cells opsonized with iC3b via anti-tumor Abs. Despite evidence for priming of macrophage CR3 by oral beta-glucan in vivo, the current study in C57BL/6 and BALB/c mice showed that granulocytes were the essential killer cells in mAb- and oral beta-glucan-mediated tumor regression, because responses were absent in granulocyte-depleted mice. Among granulocytes, neutrophils were the major effector cells, because tumor regression did not occur when C5a-dependent chemotaxis was blocked with a C5aR antagonist, whereas tumor regression was normal in C3aR(-/-) mice. Neutrophil recruitment by C5a in vivo required amplification via leukotriene B-4, because both C5a-mediated leukocyte recruitment into the peritoneal cavity and tumor regression were suppressed in leukotriene B4R-deficient (BLT-1(-/-)) mice.
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