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Monocyte exhaustion mediated by TRAM

ABSTRACT: Monocyte exhaustion mediated by TRAM

PROVIDER: PRJNA755992 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15510606.fastq.gz	Fastqsanger.gz
	SRR15510607.fastq.gz	Fastqsanger.gz
	SRR15510608.fastq.gz	Fastqsanger.gz

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Monocyte exhaustion mediated by TRAM

Project description:We performed single cell sequencing analysis of exhausted monocytes generated in vitro through prolonged incubation with high dose LPS. We demonstated that 5-day prolonged stimulation of WT but not TRAM KO monocytes with high dose LPS drastically induced monocyte exhaustion, as reflected in higher levels of inflammatory marker genes such as CD38 and immuno-suppressor genes including PD-L1.

2021-10-22 | GSE182355 | GEO

Alleviation of monocyte exhaustion by BCG derivative mycolic acid

Project description:Monocyte exhaustion characterized by sustained pathogenic inflammatory and immune-suppressive features underlies the pathogenesis of sepsis induced by systemic polymicrobial infections. However, effective strategies in blocking monocyte exhaustion and restoring innate homeostasis are currently not available. In this study, we found that Methoxy-Mycolic Acid (M-MA), a branched mycolic acid derived from Mycobacterium Bovis Bacillus Calmette–Guérin (BCG), to be a potent agent in alleviating monocyte exhaustion and restoring immune homeostasis. Co-treatment of monocytes with M-MA can effectively block the expansion of exhausted Ly6Chi /CD38hi/PD-L1hi monocytes induced by repetitive LPS challenges, and restore the expression of immune-enhancing CD86 on co-treated monocytes. Functionally, M-MA treatment restored mitochondrial functions of exhausted monocytes and alleviated their suppressive activities on co-cultured T cells. Mechanistically, M-MA exerts its protective effects independent of cellular receptor TREM2, and relieves cellular stress signaling through blocking Src-STAT1 mediated pathogenic inflammatory polarization as well as reducing the production of compensatory immune suppressors TAX1BP1 and PLAC8. Our whole genome methylation analyses further revealed that M-MA can effectively erase methylation memory of exhausted monocytes, with validated restoration of plac8 methylation by M-MA. Together, our data reveal M-MA as a potent agent in restoring monocyte homeostasis with future therapeutic potential for the treatment of sepsis.

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Alleviation of monocyte exhaustion by BCG derivative mycolic acid

Project description:Alleviation of monocyte exhaustion by BCG derivative mycolic acid

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Project description:Altered DNA methylation underlies monocyte dysregulation and immune exhaustion memory in sepsis

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Lymphopenia-induced T cell exhaustion in STING gain-of-function mouse model

Project description:STING gain-of-function (GOF) mutations lead to T cell lymphopenia, in the context of severe combined immunodeficiency (SCID) for STING GOF V154M mice. This T cell lymphopenia, which is of central origin, has been described as type I IFN independent and associated with dysfunctions of the rare mature T cells found in the periphery. To better describe the biological mechanisms of these dysfunctions, we performed a transcriptomic analysis by RNA-seq on sorted splenic CD4+ and CD8+ mature T cells from STING GOF mice. We highlighted an unexpected T cell exhaustion phenotype that could partly explain their dysfunctions. Acquired very early in life, but only once the peripheral environment is reached, the phenotype appeared to depend neither on type I IFNs, nor on the intrinsic activation of STING in T or stromal cells. Mechanistically, the few mature T cells reaching the periphery seem to be rapidly impacted by the lymphopenic environment through increased antigenic and IL-7 stimulations that could lead to their exhaustion. By using STING GOF long term-hematopoietic stem cells (LT-HSC) transplantations with supportive wild-type bone marrow (BM) cells, we prevented the T cell exhaustion of STING GOF T cells in the resulting non lymphopenic context. With the support of lymphopenic RAG1 hypomorphic mice developing the phenotype, our data uncover a lymphopenia-mediated T cell exhaustion mechanism in STING GOF mice, for which a synergistic effect of the mutation is also envisaged.

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Project description:Altered DNA methylation underlies monocyte dysregulation and immune exhaustion memory in sepsis [CUT&RUN]

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