Medicina (Kaunas) 2007; 43 (8): 597-606

Contents   Full text article in English

Effects of β-glucans on the immune system

Dalia Akramienė, Anatolijus Kondrotas, Janina Didžiapetrienė1, Egidijus Kėvelaitis

Department of Physiology, Kaunas University of Medicine, 1Institute of Oncology, Vilnius University, Lithuania

Key words: β-glucan; anticarcinogenic activity; monoclonal antibodies; complement receptor.

Summary. β-Glucans are naturally occurring polysaccharides. These glucose polymers are constituents of the cell wall of certain pathogenic bacteria and fungi. The healing and immunostimulating properties of mushrooms have been known for thousands of years in the Eastern countries. These mushrooms contain biologically active polysaccharides that mostly belong to group of β-glucans. These substances increase host immune defense by activating complement system, enhancing macrophages and natural killer cell function. The induction of cellular responses by mushroom and other β-glucans is likely to involve their specific interaction with several cell surface receptors, as complement receptor 3 (CR3; CD11b/CD18), lactosylceramide, selected scavenger receptors, and dectin-1 (βGR). β-Glucans also show anticarcinogenic activity. They can prevent oncogenesis due to the protective effect against potent genotoxic carcinogens. As immunostimulating agent, which acts through the activation of macrophages and NK cell cytotoxicity, β-glucan can inhibit tumor growth in promotion stage too. Anti-angiogenesis can be one of the pathways through which β-glucans can reduce tumor proliferation, prevent tumor metastasis. β-Glucan as adjuvant to cancer chemotherapy and radiotherapy demonstrated the positive role in the restoration of hematopiesis following by bone marrow injury. Immunotherapy using monoclonal antibodies is a novel strategy of cancer treatment. These antibodies activate complement system and opsonize tumor cells with iC3b fragment. In contrast to microorganisms, tumor cells, as well as other host cells, lack β-glucan as a surface component and cannot trigger complement receptor 3-dependent cellular cytotoxicity and initiate tumor-killing activity. This mechanism could be induced in the presence of β-glucans.

Correspondence to D. Akramienė, Department of Physiology, Kaunas University of Medicine, A. Mickevičiaus 9, 44307 Kaunas, Lithuania. E-mail:

Received 19 January 2007, accepted 6 August 2007