Particulate β-glucan regulates the immunosuppression of granulocytic myeloid-derived suppressor cells by inhibiting NFIA expression

Tian, Xinyu; Tian, Jie; Tang, Xinyi; Rui, Ke; Zhang, Yue; Ma, Jie; Wang, Yungang; Xu, Huaxi; Lu, Liwei; Wang, Shengjun

doi:10.1080/2162402x.2015.1038687

Cited by 28 publications

(27 citation statements)

References 33 publications

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“…In cancer development, MDSCs accelerate tumor progression by inhibiting the T cell response and inducing regulatory T cells by releasing arginase 1 (Arg1), reactive oxygen species (ROS), and inducible nitric oxide synthase. Currently, therapies targeting MDSCs mainly involve promoting the differentiation of MDSCs, inhibiting the suppressive effect of MDSCs or eliminating MDSCs ( 19 – 21 ).…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA HOXA Transcript Antisense RNA Myeloid-Specific 1–HOXA1 Axis Downregulates the Immunosuppressive Activity of Myeloid-Derived Suppressor Cells in Lung Cancer

et al. 2018

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HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1) is a long non-coding RNA that has been shown to be a key regulator of myeloid cell development by targeting HOXA1. Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells that possess immunosuppressive function. However, the impact of HOTAIRM1 on the development of MDSCs remains unknown. In this study, we demonstrated that HOTAIRM1 was expressed in MDSCs and that overexpression of HOTAIRM1 could downregulate the expression of suppressive molecules in MDSCs. In addition, HOTAIRM1 levels were observed to be decreased in the peripheral blood cells of lung cancer patients compared with those of healthy controls. By analyzing HOTAIRM1 expression levels in different types of lung cancer, we found that HOTAIRM1 was mainly expressed in lung adenocarcinoma. Finally, it was confirmed that HOTAIRM1 could enhance the expression of HOXA1 in MDSCs and that high levels of HOXA1, the target gene of HOTAIRM1, could delay tumor progression and enhance the antitumor immune response by downregulating the immunosuppression of MDSCs. Taken together, this study illustrates that HOTAIRM1/HOXA1 downregulates the immunosuppressive function of MDSCs and may be a potential therapeutic target in lung cancer.

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Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA HOXA Transcript Antisense RNA Myeloid-Specific 1–HOXA1 Axis Downregulates the Immunosuppressive Activity of Myeloid-Derived Suppressor Cells in Lung Cancer

et al. 2018

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“…Moreover, the immunosuppressive mechanism of G-MDSC is different from that of M-MDSC [ 10 ]. G-MDSC suppress innate and adaptive immune responses through mechanisms involving L-arginine metabolism and reactive oxygen species (ROS) production [ 11 , 12 ]. These immunosuppressive roles of G-MDSC imply that they can be used to treat autoimmune diseases [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Exosomes released by granulocytic myeloid-derived suppressor cells attenuate DSS-induced colitis in mice

et al. 2016

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Myeloid-derived suppressor cells (MDSC) have been described in inflammatory bowel disease (IBD), but their role in the disease remains controversial. We sought to define the effect of granulocytic MDSC-derived exosomes (G-MDSC exo) in dextran sulphate sodium (DSS)-induced murine colitis. G-MDSC exo-treated mice showed greater resistance to colitis, as reflected by lower disease activity index, decreased inflammatory cell infiltration damage. There was a decrease in the proportion of Th1 cells and an increase in the proportion of regulatory T cells (Tregs) in mesenteric lymph nodes (MLNs) from G-MDSC exo-treated colitis mice. Moreover, lower serum levels of interferon (IFN)-γ and tumor necrosis factor (TNF)-α were detected in G-MDSC exo-treated colitis mice. Interestingly, inhibition of arginase (Arg)-1 activity in G-MDSC exo partially abrogated the spontaneous improvement of colitis. In addition, G-MDSC exo could suppress CD4+ T cell proliferation and IFN-γ secretion in vitro and inhibit the delayed-type hypersensitivity (DTH) response, and these abilities were associated with Arg-1 activity. Moreover, G-MDSC exo promoted the expansion of Tregs in vitro. Taken together, these results suggest that G-MDSC exo attenuate DSS-induced colitis through inhibiting Th1 cells proliferation and promoting Tregs expansion.

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“…NFIA is known to regulate cell fate in the central nervous system and myeloid cells (Glasgow et al, 2014;Hiraike et al, 2017;Kang et al, 2012;Mei et al, 2016;Tian et al, 2015;Yang et al, 2018), however, the adult functions of NFIA in these cells have not yet been established. Here, we illustrate a new function of NFIA not related to cell cycle, cell fate determination, or organ formation.…”

Section: Discussionmentioning

confidence: 99%

NFIA regulates granule recruitment and exocytosis in the adult pancreas

Scavuzzo

Chmielowiec

Teaw

et al. 2019

Preprint

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After food ingestion, pancreatic cells secrete zymogen and hormone-containing granules to precisely control digestion and blood glucose levels. Identifying regulators of this process is paramount to combatting multiple pancreatic diseases. Here we show that pancreatic deletion of the transcription factor nuclear factor IA (NFIA) leads to hyperglycemia, hypoinsulinemia, and hypolipidemia. Surprisingly, insulin and digestive enzymes are produced in the absence of NFIA, however, they are not secreted properly and instead accumulate inside pancreatic cells. In NFIA-deficient mice we saw a reduction of insulin granules in the ready releasable pool and the first-phase insulin response was impaired. We found that NFIA binds to and activates Rab39b, a Rab GTPase critical for exocytosis. Re-expression of Rab39b in NFIA knockout islets restored glucose-stimulated insulin secretion. In sum, the NFIA-Rab39b axis regulates pancreatic physiology through granule recruitment and docking, linking NFIA to a new process with potential effects in diabetes, pancreatitis, and lipid disorders.

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Particulate β-glucan regulates the immunosuppression of granulocytic myeloid-derived suppressor cells by inhibiting NFIA expression

Cited by 28 publications

References 33 publications

Long Non-Coding RNA HOXA Transcript Antisense RNA Myeloid-Specific 1–HOXA1 Axis Downregulates the Immunosuppressive Activity of Myeloid-Derived Suppressor Cells in Lung Cancer

Long Non-Coding RNA HOXA Transcript Antisense RNA Myeloid-Specific 1–HOXA1 Axis Downregulates the Immunosuppressive Activity of Myeloid-Derived Suppressor Cells in Lung Cancer

Exosomes released by granulocytic myeloid-derived suppressor cells attenuate DSS-induced colitis in mice

NFIA regulates granule recruitment and exocytosis in the adult pancreas

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