Aim:To study the effects(and the mechanisms thereof)of Ganoderma lucidumpolysaccharides(G/-PS)on the proliferation and the anti-tumor activity of cytokine-induced killer(CIK)cells,and to make use of CIK cells as a means to investigatethe interactions between Gl-PS and cytokines.Methods:CIK cells were preparedby using the standard protocol as a positive control.Experimental groups alsounderwent the standard protocol,except that Gl-PS(400 mg/L or 100 mg/L)wasadded and the dose of anti-CD3 and interleukin-2 they received was reduced by50% and 75%,respectively.For negative controls,Gl-PS in the experimentalprotocol was replaced with soluble starch or methylcellulose(400 mg/L or 100 mg/L).CIK cell proliferation,cytotoxicity,and phenotype were determined by using theTrypan blue exclusion method,MTT assay,and flow cytometry.Results:Bysynergizing cytokines,Gl-PS(400 mg/L or 100 mg/L)could decrease the amountof cytokine in lymphokine activated killer(LAK)cells and CIK cells culture,buthad no significant effect on the proliferation,cytotoxicity,or phenotype of LAKcells,or CIK cells induced by cytokines at higher doses alone,in which CIK cellsexpanded about 80-fold and the main effectors,CD3~+NK1.1~+ cells,expanded bymore than 15%.The cytotoxicity of CIK cells in experimental groups was 79.3%±4.7%,76.9%±6.8% versus the positive control 80.7%±6.8% against P815(P>0.05)and 88,9%±5.5%,84.7%±7.9% versus the positive control 89.8%±4.5% againstYAC-1(P>0.05).The activity of GI-PS could mostly be blocked by anti-CR3.Conclusion:GI-PS was shown to be a promising biological response modifier andimmune potentiator.The effect of GI-PS on CIK cells is possibly mediated prima-rily through complement receptor type 3. Aim: To study the effects (and the mechanisms thereof) of Ganoderma lucidum polysaccharides (G/-PS) on the proliferation and the anti-tumor activity of cytokine-induced killer (CIK) cells, and to make use of CIK cells as a means To investigate the interactions between Gl-PS and cytokines.Methods: CIK cells were prepared by using the standard protocol as a positive control.Experimental groups also underwent the standard protocol,except that Gl-PS (400 mg/L or 100 mg/L)wasadded and The dose of anti-CD3 and interleukin-2 they received was reduced by50% and 75%, respectively.For negative controls,Gl-PS in the experimentalprotocol was replaced with soluble starch or methylcellulose (400 mg/L or 100 mg/L) .CIK cell proliferation,cytotoxicity,and phenotype were determined by using the Trypan blue exclusion method,MTT assay,and flow cytometry.Results:Bysynergizing cytokines,Gl-PS (400 mg/L or 100 mg/L)could decrease the amount of cytokine in Lymphokine activated killer(LAK)cells and CIK cells culture,buthad no si Gnificant effect on the proliferation,cytotoxicity, or phenotype of LAKcells,or CIK cells induced by cytokines at higher doses alone, in which CIK cellsexpanded about 80-fold and the main effectors,CD3~+NK1.1~+ cells,expanded bymore than 15%.The cytotoxicity of CIK cells in experimental groups was 79.3%±4.7%,76.9%±6.8% versus the positive control 80.7%±6.8% against P815(P>0.05) and 88,9%±5.5%,84.7% ±7.9% versus the positive control 89.8%±4.5% againstYAC-1(P>0.05).The activity of GI-PS could mostly be blocked by anti-CR3.Conclusion:GI-PS was shown to be a promising biological response modifier Andimmune potentiator.The effect of GI-PS on CIK cells is possibly mediated prima-rily through complement receptor type 3.