Beta-glucans, biological response modifiers (BRMs) derived from the cell walls of yeast and other sources, have been demonstrated to prime leukocyte complement receptor 3 (CR3), thus enabling these cells to kill tumours opsonised with complement fragment iC3b. Many tumours activate complement via the classical pathway mediated by antitumour monoclonal antibodies (mAbs) or natural antibodies. Studies into the cellular and molecular mechanisms of action have demonstrated that orally administrated yeast beta-glucans are ingested and processed by macrophages. These macrophages secrete the active moiety that primes neutrophil CR3 to kill iC3b-opsonised tumour cells. Extensive studies in preclinical animal tumour models have demonstrated the efficacy of combined oral particulate yeast beta-glucan with antitumour mAb therapy in terms of tumour regression and long-term survival. It is proposed that the addition of beta-glucan will further improve the clinical therapeutic efficacy of antitumour mAbs in cancer patients.