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    Area of Science:

    • Immunology
    • Cell Biology
    • Glycobiology

    Background:

    • T cells are key to adaptive immunity, with their persistence regulated by programmed cell death pathways.
    • Tumor Necrosis Factor (TNF) receptor superfamily members mediate cell death, and their function can be modulated by sialoglycans.
    • Sialoglycans on cell death receptors are known to attenuate apoptotic functions, acting as a pro-survival mechanism in cancer, but their role in T cells is unknown.

    Purpose of the Study:

    • To investigate the role of sialoglycans in regulating programmed cell death of human T cells.
    • To explore the impact of sialoglycan deficiency on Fas receptor (FasR) activity and associated signaling pathways.
    • To determine if sialoglycans are immunophysiological regulators of T cell death.

    Main Methods:

    • Utilized immortalized (Jurkat) and primary human T cells deficient in sialoglycans.
    • Assessed apoptosis induced by Fas receptor (FasR), TNFR1, and TRAIL-R1.
    • Analyzed FasR dynamic reorganization and employed phosphoproteomics to study signaling pathways.
    • Used a sialic acid-cleaving enzyme (sialidase) on primary human T cells.

    Main Results:

    • T cell sialoglycans specifically suppressed Fas receptor-induced apoptosis, but not that of TNFR1 or TRAIL-R1.
    • Sialoglycan deficiency increased FasR dynamic reorganization, indicating glycans limit receptor clustering.
    • Loss of sialoglycans negatively regulated the pro-survival MAPK/ERK signaling pathway.
    • Sialidase treatment confirmed sialoglycans as regulators of FasR-driven cell death in primary T cells.

    Conclusions:

    • Sialoglycans on T cells are critical regulators of Fas receptor-mediated programmed cell death.
    • The T cell glycocalyx, specifically sialoglycans, influences cell fate decisions via the Fas pathway.
    • These findings provide a basis for understanding the immunoregulatory roles of the glycocalyx and its therapeutic potential in T cell-based therapies.