Imprime PGG, a yeast β-glucan immunomodulator, has the potential to repolarize human monocyte-derived M2 macrophages to M1 phenotype

Chan, Anissa; Qiu, Xiaohong; Jonas, Adria Bykowski; Patchen, Myra L.; Bose, Nandita

doi:10.1186/2051-1426-2-s3-p191

Cited by 15 publications

(13 citation statements)

References 4 publications

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“…An example is BTH1677, a fungal-derived 1,3-1,6 beta-glucan, which increased direct killing of antibody-targeted tumor cells by macrophages in vitro, through Fcγ receptors and complement receptor 3 (CR3) [82]. BTH1677 also repolarized M2-like to M1-like TAMs in vitro and enhanced CD4 T cell proliferation and IFN-γ production [83]. Furthermore, BTH1677 demonstrated synergistic antitumor effects with anti-PD-1 and PD-L1 antibodies in a 4 T1 tumor bearing mouse model [84].…”

Section: Immunotherapymentioning

confidence: 99%

Tumor-associated macrophages in breast cancer: Innocent bystander or important player?

Qiu

Waaijer

Zwager

et al. 2018

Cancer Treatment Reviews

354

287

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Tumor-associated macrophages (TAMs) are important tumor-promoting cells in the breast tumor microenvironment. Preclinically TAMs stimulate breast tumor progression, including tumor cell growth, invasion and metastasis. TAMs also induce resistance to multiple types of treatment in breast cancer models. The underlying mechanisms include: induction and maintenance of tumor-promoting phenotype in TAMs, inhibition of CD8+ T cell function, degradation of extracellular matrix, stimulation of angiogenesis and inhibition of phagocytosis. Several studies reported that high TAM infiltration of breast tumors is correlated with a worse patient prognosis. Based on these findings, macrophage-targeted treatment strategies have been developed and are currently being evaluated in clinical breast cancer trials. These strategies include: inhibition of macrophage recruitment, repolarization of TAMs to an antitumor phenotype, and enhancement of macrophage-mediated tumor cell killing or phagocytosis. This review summarizes the functional aspects of TAMs and the rationale and current evidence for TAMs as a therapeutic target in breast cancer.

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Section: Immunotherapymentioning

confidence: 99%

Tumor-associated macrophages in breast cancer: Innocent bystander or important player?

Qiu

Waaijer

Zwager

et al. 2018

Cancer Treatment Reviews

354

287

View full text Add to dashboard Cite

show abstract

“…This enhanced T cell activity results from β-glucan induced IFN-β production by DCs, which enhances the production of IFN-γ and Granzyme-B by CD8 + T cells (171). While β-glucans are commonly consumed by humans in foods prepared with yeast, care needs to be taken when considering their use for inducing TRIM in SARS-CoV-2 patients, as some studies have shown that β-glucans enhance M1 polarization of AMs -a phenomenon that may enhance the cytokine storm induced by SARS-CoV-2 (172,173).…”

Section: Trained Immunity: a Defense Against Covid-19?mentioning

confidence: 99%

Covid-19: Perspectives on Innate Immune Evasion

et al. 2020

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The ongoing outbreak of Coronavirus disease 2019 infection achieved pandemic status on March 11, 2020. As of September 8, 2020 it has caused over 890,000 mortalities worldwide. Coronaviral infections are enabled by potent immunoevasory mechanisms that target multiple aspects of innate immunity, with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) able to induce a cytokine storm, impair interferon responses, and suppress antigen presentation on both MHC class I and class II. Understanding the immune responses to SARS-CoV-2 and its immunoevasion approaches will improve our understanding of pathogenesis, virus clearance, and contribute toward vaccine and immunotherepeutic design and evaluation. This review discusses the known host innate immune response and immune evasion mechanisms driving SARS-CoV-2 infection and pathophysiology.

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“…The BTH1677/ABA/iC3b complex initially binds to innate immune effector cells through complement receptor 3 and Fc gamma receptor IIA (FcγIIA) [ 17 , 18 ], activating innate immune cells and enabling direct killing of antibody-targeted tumor cells [ 17 ]. BTH1677 also enables remodeling of the tumor microenvironment, shifting the normally suppressive M2-state macrophages to a more M1 (pro-inflammatory) state [ 19 – 21 ], and promoting depletion and/or maturation of myeloid-derived suppressor cells in the tumor microenvironment [ 22 , 23 ]. BTH1677 additionally activates antigen-presenting cells, driving co-stimulatory marker expression on macrophages and dendritic cells, as well as dendritic cell maturation, CD4 and CD8 T-cell expansion, and production of key anti-tumor cytokines (e.g., interferon gamma) [ 20 , 24 – 27 ].…”

Section: Introductionmentioning

confidence: 99%

A randomized, controlled trial evaluating the efficacy and safety of BTH1677 in combination with bevacizumab, carboplatin, and paclitaxel in first-line treatment of advanced non-small cell lung cancer

Engel-Riedel¹,

Lowe²,

Mattson³

et al. 2018

j. immunotherapy cancer

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BackgroundBTH1677, a beta-glucan pathogen-associated molecular pattern molecule, drives an anti-cancer immune response in combination with oncology antibody therapies. This phase II study explored the efficacy, pharmacokinetics (PK), and safety of BTH1677 combined with bevacizumab/carboplatin/paclitaxel in patients with untreated advanced non-small cell lung cancer (NSCLC).MethodsPatients were randomized to the BTH1677 arm (N = 61; intravenous [IV] BTH1677, 4 mg/kg, weekly; IV bevacizumab, 15 mg/kg, once each 3-week cycle [Q3W]; IV carboplatin, 6 mg/mL/min Calvert formula area-under-the-curve, Q3W; and IV paclitaxel, 200 mg/m2, Q3W) or Control arm (N = 31; bevacizumab/carboplatin/paclitaxel as above). Carboplatin/paclitaxel was discontinued after 4-6 cycles and patients who responded or remained stable received maintenance therapy with BTH1677/bevacizumab (BTH1677 arm) or bevacizumab (Control arm). Efficacy assessments, based on blinded central radiology review, included objective response rate (ORR; primary endpoint), disease control rate, duration of objective response, and progression-free survival. Overall survival and adverse events (AEs) were also assessed.ResultsORR was higher in the BTH1677 vs Control arm but the difference between groups was not statistically significant (60.4% vs 43.5%; P = .2096). All other clinical endpoints also favored the BTH1677 arm but none statistically differed between arms. PK was consistent with previous studies. Although a higher incidence of Grade 3/4 AEs occurred in the BTH1677 vs Control arm (93.2% vs 66.7%), no unexpected AEs were observed. Serious AEs and discontinuations due to AEs were lower in the BTH1677 vs Control arm.ConclusionsImprovements in tumor assessments and survival were observed with BTH1677/bevacizumab/carboplatin/paclitaxel compared with control treatment in patients with advanced NSCLC.Trial registrationClinicalTrials.gov registration ID: NCT00874107. Registered 2 April 2009. First participant was enrolled on 29 September 2009.

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Imprime PGG, a yeast β-glucan immunomodulator, has the potential to repolarize human monocyte-derived M2 macrophages to M1 phenotype

Cited by 15 publications

References 4 publications

Tumor-associated macrophages in breast cancer: Innocent bystander or important player?

Tumor-associated macrophages in breast cancer: Innocent bystander or important player?

Covid-19: Perspectives on Innate Immune Evasion

A randomized, controlled trial evaluating the efficacy and safety of BTH1677 in combination with bevacizumab, carboplatin, and paclitaxel in first-line treatment of advanced non-small cell lung cancer

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