Impact of sialyltransferase deletion in mature T cells on control of subcutaneous and metastatic cancers

Dampak delesi sialiltransferase pada sel T matang terhadap pengendalian kanker subkutan dan metastatik

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ID: 325599
2026
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Abstract
To investigate the roles of the α2,3-sialyltransferase ST3Gal1 and the α2,6-sialyltransferase ST6Gal1 in T cell-mediated tumor control, we generated mice with mature T cell-specific deletion of ST3Gal1 (T-ST3KO) or ST6Gal1 (T-ST6KO) using distal Lck-Cre-mediated recombination. Deletion of ST3Gal1 in mature T cells did not affect thymic T cell development but resulted in a reduction of peripheral CD8+ T cells. In contrast, ST6Gal1 deletion had minimal impact on T cell development and peripheral T cell abundance. Following in vitro stimulation of isolated T cells from T-ST3KO and parental wild type (WT) mice with anti-CD3 plus anti-CD28/CD80-Fc, CD8+ T cells from T-ST3KO mice exhibited enhanced activation and an increased frequency of CD44 positive memory-like T cells, while comparison of T cells from T-ST6KO and the parental WT mice showed no significant changes. Despite the activated CD8+ T cell phenotype in T-ST3KO mice, subcutaneous MC38 tumors displayed accelerated growth. In contrast, tumor progression in T-ST6KO mice was unchanged from the parental WT mice. Notably, T-ST6KO mice developed increased pulmonary metastases following intravenous challenge with B16F10 melanoma cells, whereas metastatic burden was unaffected in T-ST3KO mice. These findings demonstrate distinct and non-redundant roles for ST3Gal1- and ST6Gal1-mediated sialylation in regulating T cell function and antitumor immunity and reveal context-dependent effects of T-cell intrinsic sialylation in controlling primary tumor growth and metastatic dissemination.
Untuk menyelidiki peran α2,3-sialiltransferase ST3Gal1 dan α2,6-sialiltransferase ST6Gal1 dalam pengendalian tumor yang diperantarai sel T, kami menghasilkan mencit dengan delesi spesifik sel T matang terhadap ST3Gal1 (T-ST3KO) atau ST6Gal1 (T-ST6KO) menggunakan rekombinasi yang diperantarai Lck-Cre distal. Delesi ST3Gal1 pada sel T matang tidak memengaruhi perkembangan sel T di timus, tetapi menyebabkan penurunan sel T CD8+ perifer. Sebaliknya, delesi ST6Gal1 memiliki dampak minimal terhadap perkembangan sel T dan kelimpahan sel T perifer. Setelah stimulasi *in vitro* pada sel T terisolasi dari mencit T-ST3KO dan mencit tipe liar (*wild type*, WT) parental dengan anti-CD3 serta anti-CD28/CD80-Fc, sel T CD8+ dari mencit T-ST3KO menunjukkan aktivasi yang meningkat dan peningkatan frekuensi sel T serupa memori (*memory-like*) yang positif CD44, sedangkan perbandingan sel T dari mencit T-ST6KO dan mencit WT parental tidak menunjukkan perubahan yang signifikan. Terlepas dari fenotipe sel T CD8+ yang teraktivasi pada mencit T-ST3KO, tumor subkutan MC38 menunjukkan pertumbuhan yang dipercepat. Sebaliknya, progresi tumor pada mencit T-ST6KO tidak berubah dibandingkan dengan mencit WT parental. Khususnya, mencit T-ST6KO mengalami peningkatan metastasis paru setelah uji tantang intravena dengan sel melanoma B16F10, sedangkan beban metastasis tidak terpengaruh pada mencit T-ST3KO. Temuan ini menunjukkan peran yang berbeda dan non-redundan dari sialilasi yang diperantarai ST3Gal1 dan ST6Gal1 dalam meregulasi fungsi sel T serta imunitas antitumor, dan mengungkap efek yang bergantung pada konteks dari sialilasi intrinsik sel T dalam mengendalikan pertumbuhan tumor primer dan diseminasi metastasis.
Reference Key
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Authors Xiaoshuang Wang, James C Paulson
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Journal glycobiology
Year 2026
DOI
10.1093/glycob/cwag065
URL
https://doi.org/10.1093/glycob/cwag065
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