What question did this study set out to answer?

This research aims to investigate how ST8Sia6-dependent glycosylation affects gut inflammation and immune cell behavior.

May 17, 2026Cell Reports0 citationsOpen Access

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ST8Sia6-dependent glycosylation restrains gut inflammation and pathogenic Th1 and Th17 programs

SCSydney B. CrottsMayo Clinic JBJackson T. BarnesMayo Clinic RARegina AntonettiMayo Clinic

Key Points

This research aims to investigate how ST8Sia6-dependent glycosylation affects gut inflammation and immune cell behavior.
Utilized ST8Sia6-deficient and heterozygous mice to study immune responses
Analyzed glycosylation patterns of immune cells like T cells
Measured levels of chemokines in immune and epithelial cells
ST8Sia6-deficient T cells produce more TNF-α when stimulated in vitro
Increased chemokine levels (CCL3, CCL4, CCL5) in ST8Sia6-deficient cells
Heterozygous mice exhibited an intermediate immune response phenotype

Abstract

17 programs and readily generate TNF-α upon in vitro stimulation. In addition, there are increased levels of inflammation-induced chemokines CCL3, CCL4, and CCL5 in ST8Sia6-deficient immune and epithelial cells. ST8Sia6-deficient T cells show altered glycosylation of CD43 and CD45. ST8Sia6 heterozygous mice show an intermediate phenotype, demonstrating that gut immune homeostasis is sensitive to ST8Sia6 expression levels. This work thus establishes a role for immune cell glycosylation by ST8Sia6 in IBD.

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Cite This Study

Crotts et al. (Fri,) studied this question.

synapsesocial.com/papers/6a095ac47880e6d24efe0aae https://doi.org/https://doi.org/10.1016/j.celrep.2026.117347

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