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Effect of ApoE in communicating CD4+ T cell activation and proliferation

ABSTRACT: Effect of ApoE in communicating CD4+ T cell activation and proliferation

PROVIDER: PRJNA996509 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25338449.fastq.gz	Fastqsanger.gz
	SRR25338450.fastq.gz	Fastqsanger.gz
	SRR25338451.fastq.gz	Fastqsanger.gz
	SRR25338452.fastq.gz	Fastqsanger.gz
	SRR25338453.fastq.gz	Fastqsanger.gz

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Effect of ApoE in communicating CD4+ T cell activation and proliferation

Project description:While ApoE expression by myeloid cells is recognized to control inflammation, whether such benefits can be communicated via extracellular vesicles including exosomes is not known. Through the study of exosomes produced by macrophages derived from the bone marrow of Wildtype (WT-BMDM-exo) and ApoE deficient (EKO-BMDM-exo) mice, we uncover a critical role of ApoE in regulating cell signaling properties. We treated splenic CD4+ T cells with EKO-BMDM-exo, WT-BMDM-exo, or PBS and performed gene expression profiling analysis. We found that CD4+ T cells treated with EKO-BMDM-exo show elevations in genes involved in the T-cell receptor complex (Cd3e, Cd247, & Cd4) and Il2rg, a key component of cytokine receptors on CD4+ T cells. Taken together, our data unveil a novel property of macrophage ApoE in controlling adaptive immunity by their secreted exosomes.

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Project description:Homeostatic proliferation, driven by cytokines including IL-7, maintains stable T cell populations over time and expands these during lymphopenia, for example following stem cell transplantation. Yet, impaired T cell expansion in this context is associated with diminished immune protection, whilst excessive proliferation contributes to graft versus host disease. This highlights the need to understand molecular mechanisms regulating this process. Here, we studied the metabolic basis for IL-7-driven CD4+ T cell proliferation. We observed that IL-7 promotes glucose uptake and metabolism, including usage for nucleotide synthesis and oxidation in the tricarboxylic acid (TCA) cycle. Of note, contrary to other TCA metabolites, glucose-derived citrate does not accumulate in IL-7 treated cells, indicating diversion into other processes. In agreement, IL-7 promotes glucose-dependent histone acetylation and chromatin accessibility during proliferation. This is particularly notable at gene loci of the amino acid-sensing Ragulator complex. Consistently, expression of its subunit LAMTOR5 is promoted by IL-7 in a glucose-dependent manner. Functionally, glucose availability determined amino acid-dependent mTOR activation in CD4+ T cells, confirming integrated sensing of these nutrients. LAMTOR5 deletion impaired IL-7-mediated CD4+ T cell expansion, establishing that glycolysis in absence of Ragulator activation was insufficient to initiate this process. Clinically, CD4+ T cells isolated from patients following myeloablative autologous stem cell transplantation demonstrate coordinated upregulation of genes encoding glycolytic and TCA cycle enzymes, as well as amino acid sensing machinery and mTOR targets. Our findings uncover integrated sensing of glucose and amino acid metabolism and demonstrate its relevance during homeostatic T cell proliferation.

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GNPS - Nrf2 drives activation-driven expansion of CD4+ T-cells by modulating glucose and glutamine metabolism

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Itch attenuates CD4 T cell proliferation in mice by limiting WBP2 protein stability

Project description:To mount an anti-pathogen response, CD4 T cells must undergo rapid cell proliferation. However, poorly controlled expansion can result in diseases such as autoimmunity. One important regulator of T cell activity is the E3 ubiquitin ligase Itch. Itch deficient patients suffer from extensive autoinflammation. Similarly, Itch deficient mice exhibit inflammation characterized by high numbers of activated CD4 T cells. While the role of Itch in limiting CD4 T cell cytokine production has been extensively studied, it is less clear whether and how Itch regulates proliferation of these cells. We determined that Itch deficient CD4 T cells are hyperproliferative in vitro and in vivo, due to increased S phase entry. Whole cell proteomics analysis of Itch deficient primary mouse CD4 T cells revealed increased abundance of the -catenin co-activator WW domain binding protein 2 (WBP2). Furthermore, Itch deficient cells demonstrate increased WBP2 protein stability, and Itch and WBP2 interact in CD4 T cells. Knockdown of WBP2 in CD4 T cells caused reduced proliferation. Together, our data support that Itch attenuates CD4 T cell proliferation by promoting WBP2 degradation. This study identifies novel roles for Itch and WBP2 in regulating CD4 T cell proliferation, providing insight into how Itch may prevent inflammation.

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