Effect of glutamine supplementation on naïve CD4 T cell differentiation from CARD11 R75W mutation patients
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ABSTRACT:
PROVIDER: PRJNA1211092 | ENA |
REPOSITORIES: ENA
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Project description:CARD11 LOF mutant patients develop severe atopic phenotpes and increased T-helper 2 (Th2) cytokine production, in addition to other immunopathology. CARD11 LOF impairs lymphocyte receptor–mediated glutamine uptake—thereby reducing signaling in mTORC1. Herein, we investigate whether exogenous glutamine treatment would alleviate Th2 phenotypes of CARD11 LOF mutant T cells.
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Project description:Tumour cells adapt to nutrient deprivation in vivo, yet strategies targeting the nutrient poor microenvironment remain unexplored. We recently found, in melanoma, tumour cells often experience low glutamine levels, which induce histone hypermethylation, promote dedifferentiation, and increase resistance to BRAF inhibitors. These findings raise the possibility that increased glutamine levels can be detrimental to melanoma tumours. Here, we show that dietary glutamine supplementation significantly inhibits melanoma tumour growth, prolongs survival in transgenic mouse model, and increases sensitivity to BRAF targeted inhibitors in both melanoma xenograft and patient-derived xenograft (PDX) models. Notably, metabolomic analysis reveals that dietary uptake of glutamine effectively increases the concentration of glutamine and its downstream metabolite, αKG, in serum and tumours, without increasing biosynthetic intermediates necessary for cell proliferation. Mechanistically, we find that glutamine supplementation uniformly alters the transcriptome and suppresses expression of many melanoma-associated genes. Our data further demonstrate that increase in intra-tumoural αKG concentration, following glutamine supplementation, drives hypomethylation of H3K4me3, thereby suppressing epigenetically-activated oncogenic pathways in melanoma. Therefore, our findings provide important evidence that glutamine supplementation can serve as a potential dietary intervention to block melanoma tumour growth and sensitize tumours to targeted therapy via epigenetic reprogramming.
2020-05-14 | GSE140274 | GEO
Project description:Glutamine supplementation suppresses herpes simplex virus reactivation
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Project description:In order to investigate the molecular mechanism of CARD11 in immune cell system, we applied the RNA-seq analysis using RNA isolated from WT and CARD11 mutant (E134G and K215M) mouse spleen B cells. By comparing the transcriptome files, we found some different expressed gene involved in due to the CARD11 point mutation and in vitro RT-PCR had confirmed this result.
2020-01-27 | GSE136588 | GEO
Project description:Activation of NFkB pathway by CARD11 Cy3-labelled untreated sample and Cy5-labelled treated sample were hybridized to a Lymphochip microarray.
2010-07-01 | E-GEOD-3896 | biostudies-arrayexpress
Project description:This study aimed to clarify the role of glutamine in atherosclerosis and its participating mechanism. Forty C57BL/6J mice were divided into wild control, ApoE-/- control, glutamine+ApoE-/-control, ApoE-/- high fat diet (HFD) and glutamine+ ApoE-/- HFD groups. The degree of atherosclerosis; plasma biochemistry and protein profiles, and western blotting and untargeted metabolomics of aortic tissue were detected at 18 weeks. An in vitro study was also performed. Glutamine treatment significantly decreased the degree of aortic atherosclerosis compared with that in the ApoE-/- HFD group (p=0.03). O-GlcNAc, IL-1β, IL-1α, GLUT1 and PKM2 in the ApoE-/- HFD group were significantly higher than those in the ApoE-/- control group (p < 0.05). These differences were reversed by glutamine treatment (p < 0.05), and aggravated by OGT overexpression in the in vitro study (p < 0.05). Multiomics showed that the ApoE-/- HFD group had higher levels of oxidative stress regulatory molecules (GUAD, XDH, PSB1 and PSB4), proinflammatory regulatory molecules (myristic acid, HMGB3, vinculin, DNJC2 and SPRC) and stress granules regulatory molecules (caprin-1 and DEAR) (p < 0.05). These differences were reversed by glutamine treatment (p < 0.05). We conclude that glutamine supplementation might alleviate atherosclerosis through downregulation of O-GlcNAc, glycolysis, oxidative stress and proinflammatory pathway.
2023-05-15 | PXD042305 |
Project description:Activation of NFkB pathway by CARD11 Keywords: time series design
2006-03-30 | GSE3896 | GEO
Project description:Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)-γ inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN-γ knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN-γ producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN-γ-associated immune response and reduce the rate of reactivation of latent virus infection.
2017-08-30 | GSE95715 | GEO
Project description:Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)-γ inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN-γ knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN-γ producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN-γ-associated immune response and reduce the rate of reactivation of latent virus infection.
2017-08-30 | GSE95714 | GEO
Project description:Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)-γ inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN-γ knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN-γ producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN-γ-associated immune response and reduce the rate of reactivation of latent virus infection.
2017-08-30 | GSE95713 | GEO