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C5a-Mediated Leukotriene B₄-Amplified Neutrophil Chemotaxis Is Essential in Tumor Immunotherapy Facilitated by Anti-Tumor Monoclonal Antibody and -Glucan¹

Daniel J. Allendorf^*,, Jun Yan^2,*,, Gordon D. Ross^3,*,,, Richard D. Hansen^*, Jarek T. Baran^4,*, Krishnaprasad Subbarao^5,*, Li Wang^* and Bodduluri Haribabu^*,

^* Tumor Immunobiology Program of the James Graham Brown Cancer Center, Departments of Microbiology and Immunology and Pathology and Laboratory Medicine, University of Louisville School of Medicine, Louisville, KY 40202

Intravenous and orally administered -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 -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 -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 B₄, 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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