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Dual T cell– and B cell–intrinsic deficiency in humans

ABSTRACT: Dual T cell– and B cell–intrinsic deficiency in humans

PROVIDER: PRJNA716960 | ENA |

REPOSITORIES: ENA

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Dual T cell– and B cell–intrinsic deficiency in humans [CD4+ T cell SubSeries]

Project description:Dual T cell– and B cell–intrinsic deficiency in humans [CD4+ T cell SubSeries]

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Dual T cell– and B cell–intrinsic deficiency in humans [CD4+ T cell SubSeries]

Project description:Human RLTPR deficiency is a combined immunodeficiency affecting the CD28-responsive pathway in T cells and the BCR-responsive pathway in B cells. This SubSeries contains high throughput gene expression data from primary CD4+ T cells of patients with RLTPR deficiency and controls.

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Dual T cell– and B cell–intrinsic deficiency in humans

Project description:This SuperSeries is composed of the SubSeries listed below.

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Dual T cell- and B cell-intrinsic deficiency in humans with biallelic RLTPR mutations.

Project description:Combined immunodeficiency (CID) refers to inborn errors of human T cells that also affect B cells because of the T cell deficit or an additional B cell-intrinsic deficit. In this study, we report six patients from three unrelated families with biallelic loss-of-function mutations in RLTPR, the mouse orthologue of which is essential for CD28 signaling. The patients have cutaneous and pulmonary allergy, as well as a variety of bacterial and fungal infectious diseases, including invasive tuberculosis and mucocutaneous candidiasis. Proportions of circulating regulatory T cells and memory CD4+ T cells are reduced. Their CD4+ T cells do not respond to CD28 stimulation. Their CD4+ T cells exhibit a "Th2" cell bias ex vivo and when cultured in vitro, contrasting with the paucity of "Th1," "Th17," and T follicular helper cells. The patients also display few memory B cells and poor antibody responses. This B cell phenotype does not result solely from the T cell deficiency, as the patients' B cells fail to activate NF-?B upon B cell receptor (BCR) stimulation. Human RLTPR deficiency is a CID affecting at least the CD28-responsive pathway in T cells and the BCR-responsive pathway in B cells.

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IEC intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation

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Inhibiting tumor cell-intrinsic UBA6 by inosine augments tumor immunogenicity

Project description:Metabolic alteration influences cancer immunity. However, the role and mechanism of metabolic adaption on immune checkpoint blockade (ICB) responses remains ill-defined. Here, metabolomic profiling in mouse tumor models and cancer patients treated with ICB was performed. We found that metabolite inosine was associated with ICB sensitivity in mice and humans, and overcame ICB resistance in several mouse tumor models. Notably, inosine sensitized tumor cells to T cell-mediated cytotoxicity by amplifying tumor-intrinsic immunogenicity. Chemical proteomics further identified that inosine directly bound and inhibited ubiquitin-activating enzyme UBA6. Tumor intrinsic UBA6 loss augmented tumor immunogenicity and substituted the synergistic effect of inosine in combination with ICB. Clinically, tumor UBA6 expression negatively correlated with ICB response in cancer patients. Thus, we reveal an unappreciated function of inosine on tumor-intrinsic immunogenicity and UBA6 as a candidate target for immunotherapy.

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Latent HIV infection disrupts cell-intrinsic innate immunity

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Cancer-cell intrinsic electrical activity drives small-cell lung cancer progression

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Growth Hormone Receptor and IGF-I Deficiency is Associated with Resistance to DNA Damage and Very Low Cancer and Diabetes Incidence in Humans

Project description:Growth Hormone Receptor Deficiency (GHRD) in mice causes life span extension and a major increase in the portion of animals that die without detectable pathologies including cancer and insulin resistance. During a 22-year monitoring of a cohort of 0-88 year old Ecuadorian GHRD subjects with severe IGF-I deficiency developed we observed a single, non-lethal malignancy and no diabetes. To understand the mechanisms responsible for this low disease incidence we incubated Human Mammary Epithelial Cells (HMECs) with serum from either GHRD or control subjects. GHRD serum not only protected mammary cells against hydrogen peroxide-dependent DNA damage but also promoted cell death in severely damaged cells by a mechanism blocked by IGF-I. The gene expression or DNA damage profile in epithelial cells exposed to GHRD serum, fibroblasts lacking the IGF-I receptor, and long-lived yeast lacking homologs of IGF-I signaling genes point to stress resistance transcription factors and SOD2 as mediators of GHRD-associated protection. These results provide evidence for a role of GH and IGF-I deficiency in promoting healthy aging in humans. Primary Human Mammalian Epithelial Cells (HMECs), were cultured in HMEC medium (ScienCell) at 37oC and 5% CO2 in Poly-L-Lysine coated culture dishes (Sigma). Treatment consisted of cells being stimulated with HMEC basal medium containing either 15% GHRD serum or 15% control serum for 6 hours. Cells were then harvested and processed for RNA extraction.

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