Oral beta-glucan adjuvant therapy converts nonprotective Th2 response to protective Th1 cell-mediated immune response in mammary tumor-bearing mice

Folia Histochem Cytobiol. 2007;45(2):107-14.


Beta (1-3)-D-glucans were identified almost 40 years ago as biological response modifiers that stimulated tumor rejection. In vitro studies have shown that beta-glucans bind to a lectin domain within complement receptor type 3 (CR3), or to, more recently described dectin-1 a beta-glucan specific receptor, acting mainly on phagocytic cells. In this study, we assessed the intracellular cytokine profiles of peripheral blood lymphocytes from mice bearing mammary tumors receiving i.v. anti-tumor mAbs combined or not with whole glucan particle suspension given orally (WGP, 400 microg every 24 hours). The proportions of T cells producing IL-4 and IFNgamma were determined by flow cytometry. The proportion of T cells producing IL-4 was significantly higher in tumor-bearing mice not receiving beta-glucan-enhanced therapy. Conversely, T cells from mice undergoing beta-glucan-enhanced therapy showed increased production of the Th1 cytokine IFNgamma. The switch from a Th2 to a Th1 response after WGP therapy was possibly mediated by intestinal mucosal macrophages releasing IL-12.

MeSH terms

  • Administration, Oral
  • Animals
  • Antibodies, Monoclonal / immunology
  • Chemotherapy, Adjuvant
  • Female
  • Immunity, Cellular / immunology*
  • Immunotherapy
  • Interferon-gamma / biosynthesis
  • Interleukin-12 / biosynthesis
  • Interleukin-4 / biosynthesis
  • Macrophages / immunology
  • Mammary Neoplasms, Experimental / drug therapy*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*
  • beta-Glucans / administration & dosage*
  • beta-Glucans / therapeutic use*


  • Antibodies, Monoclonal
  • beta-Glucans
  • Interleukin-12
  • Interleukin-4
  • Interferon-gamma