- Poster presentation
- Open Access
Imprime PGG, a yeast β-glucan immunomodulator, has the potential to repolarize human monocyte-derived M2 macrophages to M1 phenotype
© Chan et al.; licensee BioMed Central Ltd. 2014
- Published: 6 November 2014
- Tumor Microenvironment
- Interferon Gamma
- Innate Immune Cell
- Antibody Treatment
Imprime PGG (IPGG) has shown promising clinical efficacy in combination with monoclonal antibody treatment of cancer . In mice, complement receptor 3 (CR3) on innate immune cells (neutrophils and macrophages) is required for IPGG's anti-tumor activity [2, 3]. In human in vitro studies, opsonized IPGG binds CR3 on neutrophils and monocytes, but only on cells from individuals with high levels of endogenous anti-β-glucan antibodies (ABA), which is also a potential biomarker for enhanced clinical response to IPGG . Although IPGG has been shown to prime circulating neutrophils and monocytes, no data is available on its effect on N1/N2 neutrophil or M1/M2 macrophage tissue counterparts that can skew the immunostimulatory vs. immunosuppressive balance of the tumor microenvironment. The objective of this study was to investigate effects of IPGG treatment on monocyte differentiation to M1 or M2 macrophages.
IPGG has the potential to affect M2 to M1 repolarization and drive Th1 polarization. This engagement of the adaptive, along with the innate, immune system suggests that exploration of IPGG in combination with immunosuppression-relieving anti-cancer agents is warranted.
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