Human TIGIT on porcine aortic endothelial cells suppresses xenogeneic macrophage-mediated cytotoxicity

Noguchi, Yuki; Maeda, Akira; Lo, Pei‐Chi; Takakura, Chihiro; Haneda, Tomoko; Kodama, Tatsuhiko; Yoneyama, Tomohisa; Toyama, Chiyoshi; Tazuke, Yuko; Okuyama, Hiroomi; Miyagawa, Shuji

doi:10.1016/j.imbio.2019.07.008

Cited by 17 publications

(18 citation statements)

References 44 publications

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“…When TIGIT-FC binds to PVR, macrophages polarize to be tolerant M2-macrophages to increase the anti-inflammatory cytokines such as IL-10 and TGF-β and decrease the proinflammatory cytokines such as IL-1β and TNF-α (129). A study by Noguchi et al (119) showed that overexpression of TIGIT FIGURE 2 | TIGIT and CD226 are detected in MSCs. CD155 and CD112 are detected in APCs.…”

Section: T-cell Immunoglobulin and Itim Domain (Tigit)mentioning

confidence: 99%

“…TIGIT/PVR seems to be a bidirectional pathway, which is widely involved in immunosuppressive responses of different immune cells, such as monocytes, macrophages, DCs, T cells, and NK cells (112,124,128). CD155 was found to be mainly expressed on APCs (112,119,129,130). When macrophages are exposed to LPS or specific pro-inflammatory cytokines, the expression of PVR on macrophages increases significantly.…”

Section: T-cell Immunoglobulin and Itim Domain (Tigit)mentioning

confidence: 99%

“…TIGIT, also known as Vstm3, VSig9, or WUCAM, is a newly identified co-inhibitory receptor by Yu et al (112). TIGIT was found to be expressed in a variety of immune cells, including NK cells, memory T cells, M2-macrophages (M2), Treg cells, tumor-infiltrating lymphocytes (TILs), and individual immunoregulatory cells (e.g., tumor cells and MSCs) (113)(114)(115)(116)(117)(118)(119). In the tumor microenvironment, the highly expressed TIGIT in TILs may cause local immune tolerance and promote cancer metastasis and progression by modulating the activation of NK cells, DCs, and T cells.…”

Section: T-cell Immunoglobulin and Itim Domain (Tigit)mentioning

confidence: 99%

“…When TIGIT-FC binds to PVR, macrophages polarize to be tolerant M2-macrophages to increase the anti-inflammatory cytokines such as IL-10 and TGF-β and decrease the pro-inflammatory cytokines such as IL-1β and TNF-α ( 129 ). A study by Noguchi et al ( 119 ) showed that overexpression of TIGIT in porcine aortic endothelial cells (PAOECs) suppressed M1-macrophage polarization. Interestingly, TIGIT was found to be expressed only on M2-macrophages but not M1 macrophage, suggesting that TIGIT expression promotes M2-polarization ( 119 ).…”

Section: Cell Surface Receptor-mediated Mscs Immunosuppressionmentioning

confidence: 99%

“…A study by Noguchi et al ( 119 ) showed that overexpression of TIGIT in porcine aortic endothelial cells (PAOECs) suppressed M1-macrophage polarization. Interestingly, TIGIT was found to be expressed only on M2-macrophages but not M1 macrophage, suggesting that TIGIT expression promotes M2-polarization ( 119 ). Surface TIGIT may likely bind to PVR on other cells and eventually affect other immune cells, such as T cells and NK cells.…”

Section: Cell Surface Receptor-mediated Mscs Immunosuppressionmentioning

confidence: 99%

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Immunosuppressive Property of MSCs Mediated by Cell Surface Receptors

Liu

Zhou

et al. 2020

Front. Immunol.

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In the past decade, mesenchymal stem cells (MSCs) tend to exhibit inherent tropism for refractory inflammatory diseases and engineered MSCs have appeared on the market as therapeutic agents. Recently, engineered MSCs target to cell surface molecules on immune cells has been a new strategy to improve MSC applications. In this review, we discuss the roles of multiple receptors (ICAM-1, Gal-9, PD-L1, TIGIT, CD200, and CXCR4) in the process of MSCs' immunosuppressive properties. Furthermore, we discuss the principles and strategies for developing receptor-regulated MSCs and their mechanisms of action and the challenges of using MSCs as immunosuppressive therapies.

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Section: T-cell Immunoglobulin and Itim Domain (Tigit)mentioning

confidence: 99%

Section: T-cell Immunoglobulin and Itim Domain (Tigit)mentioning

confidence: 99%

Section: T-cell Immunoglobulin and Itim Domain (Tigit)mentioning

confidence: 99%

Section: Cell Surface Receptor-mediated Mscs Immunosuppressionmentioning

confidence: 99%

Section: Cell Surface Receptor-mediated Mscs Immunosuppressionmentioning

confidence: 99%

See 3 more Smart Citations

Immunosuppressive Property of MSCs Mediated by Cell Surface Receptors

Liu

Zhou

et al. 2020

Front. Immunol.

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Noncoding RNA 886 alleviates tumor cellular immunological rejection in host C57BL/C mice

Wang

Zhou

et al. 2020

Cancer Medicine

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Non‐coding RNA 886 (nc886/VTRNA2‐1) is a Pol III transcript and an atypical imprinted gene. Its exact function as a negative regulator of protein kinase R establishes its connection with innate immunity. Studies have shown that nc886 silencing is closely associated with prostate cancer progression. Previous work has constructed a cell model of stable nc886 overexpression (“mimic” or “nc886 + ”) in PC‐3M‐1E8 cell lines (1E8), which are highly bone‐metastatic human prostate cancer cells with low expression of nc886, and cells expressing the mimic were validated to have lower invasive and metastatic abilities than cells expressing the scramble transcript in vitro and in vivo. In this study, we directly injected mimic or scramble cells into the left ventricle of C57BL/C mice, an immunocompetent animal model, to elucidate the immune mechanisms of tumor‐host interactions. Interestingly, we found that tumor cells induced the inflammation of many important organs due to xenogeneic antigen rejection; this inflammation was ultimately repaired by tissue fibrosis after 28 days, except for in the spleen. The reason is that mimic cells, as heterogeneous antigens, are mostly directly recognized by macrophages or T cells in blood, and few mimic cells enter the spleen compared with scramble cells. The induction of splenic macrophage polarization to M2 macrophages by scramble cells is a critical factor in maintaining chronic splenic inflammation. In addition, we recognize that nc886 broadly decreases the expression of some human leukocyte antigen molecules and antigen transporters. This evidence reveals the interesting role of nc886 in regulating tumor cell antigens.

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Celastrol acts as a new histone deacetylase inhibitor to inhibit colorectal cancer cell growth via regulating macrophage polarity

Wang

Chen

et al. 2022

Cell Biology International

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The tumorigenesis and progression of colorectal cancer are closely related to the tumor microenvironment, especially inflammatory response. Inhibitors of histone deacetylase (HDAC) have been reported as epigenetic regulators of the immune system to treat cancer and inflammatory diseases and our results demonstrated that Celastrol could act as a new HDAC inhibitor. Considering macrophages as important members of the tumor microenvironment, we further found that Celastrol could influence the polarization of macrophages to inhibit colorectal cancer cell growth. Specially, we used the supernatant of HCT116 and SW480 cells to induce Ana-1 cells in vitro and chose the spontaneous colorectal cancer model APC min/+ mice as an animal model to validate in vivo. The results indicated that Celastrol could reverse the polarization of macrophages from M2 to M1 through impacting the colorectal tumor microenvironment both in vitro and in vivo. Furthermore, using bioinformatics analysis, we found that Celastrol might mechanistically polarize the macrophages through MAPK signaling pathway. In conclusion, our findings identified that Celastrol as a new HDAC inhibitor and suggested that Celastrol could modulate macrophage polarization, thus inhibiting colorectal cancer growth, which may provide some novel therapeutic strategies for colorectal cancer.

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Human TIGIT on porcine aortic endothelial cells suppresses xenogeneic macrophage-mediated cytotoxicity

Cited by 17 publications

References 44 publications

Immunosuppressive Property of MSCs Mediated by Cell Surface Receptors

Immunosuppressive Property of MSCs Mediated by Cell Surface Receptors

Noncoding RNA 886 alleviates tumor cellular immunological rejection in host C57BL/C mice

Celastrol acts as a new histone deacetylase inhibitor to inhibit colorectal cancer cell growth via regulating macrophage polarity

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