Pivotal regulators of tissue homeostasis and cancer: macrophages

Chen, Yulei; Zhang, Xiaobo

doi:10.1186/s40164-017-0083-4

Cited by 47 publications

(34 citation statements)

References 83 publications

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“…In allogeneic organ transplantation, ;50% of immune cells that infiltrate graft tissue are macrophages (40). Depending on the levels of proinflammatory factors that can be induced in a specific microenvironment, macrophages can change their phenotypes and biologic functions, polarizing to M1 or M2 macrophages (41). Many miRNAs are involved in macrophage polarization.…”

Section: Discussionmentioning

confidence: 99%

ADAR1 attenuates allogeneic graft rejection by suppressing miR‐21 biogenesis in macrophages and promoting M2 polarization

Liu¹,

Xie²,

Liu³

et al. 2018

FASEB j.

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ADAR1 (adenosine deaminase acting on double-stranded RNA 1) is an RNA-editing enzyme that mediates adenosine-to-inosine RNA editing events, an important post-transcriptional modification mechanism that can alter the coding properties of mRNA or regulate microRNA biogenesis. ADAR1 also regulates the innate immune response. Here, we have demonstrated that ADAR1 expression increased in LPS-stimulated macrophages. Silencing ADAR1 by using small interfering RNA in macrophages resulted in the pronounced polarization of macrophages to M1, whereas ADAR1 overexpression promoted M2 polarization, which indicated that ADAR1 can inhibit macrophage hyperpolarization and prevent immune hyperactivity. The RNA-RNP immunoprecipitation binding assay demonstrated a direct interaction between ADAR1 and miR-21 precursor. Significant up-regulation in IL-10 and down-regulation in miR-21 were observed in ADAR1-overexpressing macrophages. We evaluated miR-21 target mRNAs and macrophage polarization signaling pathways and found that forkhead box protein O1 (Foxo1) was up-regulated in cells that overexpressed ADAR1. In a mouse allogeneic skin transplantation model, grafts in the ADAR1-overexpressed group survived longer and suffered less immune cell infiltration. In ADAR1-overexpressed recipients, splenic macrophages were significantly polarized to M2, and levels of sera IL-10 were markedly higher than those in the control group. In summary, ADAR1 modulates macrophage M2 polarization via the ADAR1-miR-21-Foxo1-IL-10 axis, thereby suppressing allogeneic graft rejection.-Li, J., Xie, J., Liu, S., Li, X., Zhang, D., Wang, X., Jiang, J., Hu, W., Zhang, Y., Jin, B., Zhuang, R., Yin, W. ADAR1 attenuates allogeneic graft rejection by suppressing miR-21 biogenesis in macrophages and promoting M2 polarization.

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Section: Discussionmentioning

confidence: 99%

ADAR1 attenuates allogeneic graft rejection by suppressing miR‐21 biogenesis in macrophages and promoting M2 polarization

Liu¹,

Xie²,

Liu³

et al. 2018

FASEB j.

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“…Macrophages are highly heterogeneous immune cells that are primarily phagocytic in nature and involved in host defense and tissue remodeling ( 89 ). In response to inflammation and various other environmental stimuli, a plethora of macrophage phenotypes can be induced, which can be generally classified into two main phenotypes based on their gene expression profiles ( 90 ).…”

Section: Tams In Neuroblastomamentioning

confidence: 99%

“Re-educating” Tumor Associated Macrophages as a Novel Immunotherapy Strategy for Neuroblastoma

Liu

Joshi

2020

Front. Immunol.

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Neuroblastoma is the most common extracranial pediatric tumor and often presents with metastatic disease, and patients with high-risk neuroblastoma have survival rates of ~50%. Neuroblastoma tumorigenesis is associated with the infiltration of various types of immune cells, including myeloid derived suppressor cells, tumor associated macrophages (TAMs), and regulatory T cells, which foster tumor growth and harbor immunosuppressive functions. In particular, TAMs predict poor clinical outcomes in neuroblastoma, and among these immune cells, TAMs with an M2 phenotype comprise an immune cell population that promotes tumor metastasis, contributes to immunosuppression, and leads to failure of radiation or checkpoint inhibitor therapy. This review article summarizes the role of macrophages in tumor angiogenesis, metastasis, and immunosuppression in neuroblastoma and discusses the recent advances in “macrophage-targeting strategies” in neuroblastoma with a focus on three aspects: (1) inhibition of macrophage recruitment, (2) targeting macrophage survival, and (3) reprogramming of macrophages into an immunostimulatory phenotype.

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“…Macrophages exhibit significant plasticity and can alter their phenotype to suit their environment and function [2]. Macrophage polarisation typically produces two phenotypes; a classical pathogen-clearing pro-inflammatory 'M1' , or, an alternativelyactivated anti-inflammatory 'M2' phenotype [3,4]. To enhance pathogen clearance, macrophages can utilize the IL-1β and IL-18producing inflammasome-an intracellular multiprotein complex essential for innate immune response [5,6].…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus and Bifidobacterium Promote Antibacterial and Antiviral Immune Response in Human Macrophages

Ts¹,

Plummer²,

Aa³

et al. 2018

J Prob Health

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Objective: The objective of this study was to identify the immunomodulatory potential of two consortia of lactic acid bacteria, "Lab4" and "Lab4b", using human macrophages as an in vitro model system. Methods: THP-1 monocyte-derived macrophages were exposed to metabolites of Lab4 or Lab4b. RT-qPCR was performed on macrophages to determine the expression of M1 pro-inflammatory (IL-1β, IL-18 and CD80) or M2 antiinflammatory (CD206) marker mRNA in addition to IL-1β protein and inflammasome (NLRP3, Caspase-1, NLRP1, NLRC4 and AIM2) mRNA expression. Bacterial (LPS and ATP) and viral (Poly I:C) challenge were simulated to determine the potential of these consortia to regulate IL-1β protein, inflammasome mRNA expression, and antiviral IL-12 mRNA expression and protein under inflammatory conditions. The ability of these consortia to modulate macrophage phagocytosis of E. coli was also assessed. Results: Lab4 and Lab4b metabolites promoted an M1 phenotype in macrophages in vitro by increasing mRNA expression of IL-1β, IL-18, and CD80 and reducing mRNA expression of CD206. Induction of IL-1β protein suggested involvement of the inflammasome. mRNA expression of NLRP3, Caspase-1, NLRP1 and AIM2 was induced by Lab4 and mRNA expression of NLRP3 and Caspase-1 was induced by Lab4b suggesting different potential modes of action of the two consortia. Lab4 and Lab4b metabolites, in combination with this LPS and ATP challenge, enhanced IL-1β mRNA and protein expression further, accompanied by different mRNA expression profiles of inflammasome genes by the two consortia. Lab4 and Lab4b also induced expression of mRNA and protein of the antiviral response gene, IL-12. In combination with Poly I:C challenge, Lab4 induced IL-12 protein further, while Lab4b induced IL-12p25/IL-12p40 mRNA further highlighting potential differences. Both consortia were also able to induce phagocytosis of E. coli particles. Conclusion: Data generated from this study suggest the potential for organism-dependent control of the immunoregulatory response seen in human macrophages.

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Pivotal regulators of tissue homeostasis and cancer: macrophages

Cited by 47 publications

References 83 publications

ADAR1 attenuates allogeneic graft rejection by suppressing miR‐21 biogenesis in macrophages and promoting M2 polarization

ADAR1 attenuates allogeneic graft rejection by suppressing miR‐21 biogenesis in macrophages and promoting M2 polarization

“Re-educating” Tumor Associated Macrophages as a Novel Immunotherapy Strategy for Neuroblastoma

Lactobacillus and Bifidobacterium Promote Antibacterial and Antiviral Immune Response in Human Macrophages

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