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-1,3-Glucans Enhance the Tumoricidal Activity of Antitumor Monoclonal Antibodies in Murine Tumor Models1
* Tumor Immunobiology Program of the James Graham Brown Cancer Center, Department of Microbiology and Immunology, Department of Pathology and Laboratory Medicine, University of Louisville School of Medicine, Louisville, KY 40202;
Biopolymer Engineering, Inc., Eagan, MN 55121;
Cancer Immunotherapy Laboratory, Austin Research Institute, Victoria University of Technology, Heidelberg, Victoria, Australia; and
Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, NY 10021
Antitumor mAb bind to tumors and activate complement, coating tumors with iC3b. Intravenously administered yeast 
-1,3;1,6-glucan functions as an adjuvant for antitumor mAb by priming the inactivated C3b (iC3b) receptors (CR3; CD11b/CD18) of circulating granulocytes, enabling CR3 to trigger cytotoxicity of iC3b-coated tumors. Recent data indicated that barley -1,3;1,4-glucan given orally similarly potentiated the activity of antitumor mAb, leading to enhanced tumor regression and survival. This investigation showed that orally administered yeast -1,3;1,6-glucan functioned similarly to barley -1,3;1,4-glucan with antitumor mAb. With both oral -1,3-glucans, a requirement for iC3b on tumors and CR3 on granulocytes was confirmed by demonstrating therapeutic failures in mice deficient in C3 or CR3. Barley and yeast -1,3-glucan were labeled with fluorescein to track their oral uptake and processing in vivo. Orally administered -1,3-glucans were taken up by macrophages that transported them to spleen, lymph nodes, and bone marrow. Within the bone marrow, the macrophages degraded the large -1,3-glucans into smaller soluble -1,3-glucan fragments that were taken up by the CR3 of marginated granulocytes. These granulocytes with CR3-bound -1,3-glucan-fluorescein were shown to kill iC3b-opsonized tumor cells following their recruitment to a site of complement activation resembling a tumor coated with mAb.
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