C5a-mediated leukotriene B4-amplified neutrophil chemotaxis is essential in tumor immunotherapy facilitated by anti-tumor monoclonal antibody and beta-glucan
In: Journal of immunology (Baltimore, Md. : 1950), Jg. 174 (2005-05-21), Heft 11
Online
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Zugriff:
Intravenous and orally administered β-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 β-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 β-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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C5a-mediated leukotriene B4-amplified neutrophil chemotaxis is essential in tumor immunotherapy facilitated by anti-tumor monoclonal antibody and beta-glucan
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Autor/in / Beteiligte Person: | Baran, Jarek ; Yan, Jun ; Hansen, Richard ; Allendorf, Daniel J. ; Subbarao, Krishnaprasad ; Haribabu, Bodduluri ; Wang, Li ; Ross, Gordon D. |
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Zeitschrift: | Journal of immunology (Baltimore, Md. : 1950), Jg. 174 (2005-05-21), Heft 11 |
Veröffentlichung: | 2005 |
Medientyp: | unknown |
ISSN: | 0022-1767 (print) |
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