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Suppression of Established T Cell Immunity and Disease by Immunotherapy with Synthetically Glycosylated Antigen

ABSTRACT: The purpose of this study was to conduct an in-depth analysis of the molecular characteristics of both CD4 and CD8 T cells upon encounter of self-associated antigen presented by hepatic APCs, induce therapeutic tolerance in transgenic and endogenous repertoires of T cells, and discover the mechanisms that mediate pGal-induced tolerance.

ORGANISM(S): Mus musculus

PROVIDER: GSE192671 | GEO | 2023/09/01

REPOSITORIES: GEO

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Suppression of Established T Cell Immunity and Disease by Immunotherapy with Synthetically Glycosylated Antigen

Project description:Suppression of Established T Cell Immunity and Disease by Immunotherapy with Synthetically Glycosylated Antigen

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Repeated stimulation of self-presentation pathway by targeting erythrocytes in vivo drives anergy and profound T cell dysfunction

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Lymph Node-Targeted Synthetically Glycosylated Antigen Leads to Antigen-Specific Immunological Tolerance.

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Reprogramming Cancer into Antigen Presenting Cells as a Novel Immunotherapy [human]

Project description:Therapeutic cancer vaccination seeks to elicit activation of tumor-reactive T cells capable of recognizing tumor-associated antigens (TAAs) and eradicating malignant cells. Here, we present a cancer vaccination approach utilizing myeloid lineage reprogramming to directly convert cancer cells into tumor reprogrammed-APCs (TR-APCs). Using syngeneic murine leukemia models, we demonstrate that TR-APCs acquire both myeloid phenotype and function, process and present endogenous TAAs, and potently stimulate TAA-specific CD4+ and CD8+ T cells. In vivo TR-APC induction elicits clonal expansion of cancer-specific T cells, establishes cancer-specific immune memory, and ultimately promotes leukemia eradication. We further show that both hematologic cancers and solid tumors, including sarcomas and carcinomas, are amenable to myeloid-lineage reprogramming into TR-APCs. Finally, we demonstrate the clinical applicability of this approach by generating TR-APCs from primary clinical specimens and stimulating autologous patient-derived T cells. Thus, TR-APCs represent a cancer vaccination therapeutic strategy with broad implications for clinical immuno-oncology.

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Classical dendritic cells are required for dietary antigen-mediated peripheral regulatory T cell and tolerance induction II

Project description:Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naÃ¯ve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11bÂ¬â?? cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11bâ?? cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development. Sorted naÃ¯ve CD45.1 OT-II CD4 T cells were co-cultured with four dendritic cell subpopulations sorted from mouse mesenteric lymphnodes. 24h later OT-II cells were sorted again and compared in their gene expression profile.

2016-03-28 | E-GEOD-77304 | biostudies-arrayexpress

Classical dendritic cells are required for dietary antigen-mediated peripheral regulatory T cell and tolerance induction II

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