---
title: "Alpha2,3-sialylation on human naive T cells limits bispecific engager antitumor activity"
id: "biorxiv-15-alpha2-3-sialylation-on-human-naive-t-cells-restrains-bispecific-engager"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-15-alpha2-3-sialylation-on-human-naive-t-cells-restrains-bispecific-engager"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.08.02.742298v1?rss=1"
published_at: "2026-08-06T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Alpha2,3-sialylation on human naive T cells limits bispecific engager antitumor activity
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-15-alpha2-3-sialylation-on-human-naive-t-cells-restrains-bispecific-engager
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.08.02.742298v1?rss=1)
- **Published At:** 2026-08-06T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Aberrant cell-surface sialylation (hypersialylation) is common in human cancers and promotes immune evasion; therapies using **sialidase** aim to disrupt this glyco-checkpoint. - The study examined how T cell surface sialoglycans, especially **alpha2,3-sialylation**, influence human T cell activation, proliferation, cytokine production, and killing of tumor cells mediated by bispecific T cell engagers (**TCEs**). - Enzymatic desialylation in vitro increased T cell activation markers, proliferation, cytokine secretion, and enhanced **TCE**-mediated tumor-cell killing in healthy donor PBMC co-cultures. - In ex vivo chronic lymphocytic leukemia (CLL) PBMC cultures, combining **sialidase** treatment with the CD20-directed **TCE glofitamab** augmented cytotoxic effector transcriptional programs in autologous T cells. - Single-cell RNA-seq integrated with lectin-based CITE-seq linked treatment-driven transcriptional states to lectin-defined cell-surface glycan signatures at single-cell resolution. - Naive T cells, and to a lesser degree central memory T cells, showed elevated baseline **alpha2,3-sialylation** signatures and the strongest transcriptional responses to the combination of **glofitamab** plus **sialidase**. - CD43 was identified as a major carrier of **alpha2,3-linked sialoglycans** on T cells; genetic deletion of CD43 reduced the enhancement of T cell activation produced by **sialidase** treatment. - Authors conclude that T cell surface **sialylation** is a subset-specific, cell-intrinsic restraint on human **TCE** responses and support testing **sialidase–TCE** combinations that engage less-differentiated T cell populations. - The report is a preprint and has not undergone peer review; competing interests and funding (ERC grant 955575) are disclosed in the source.
## Clinical Analysis & Structured Key Points
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Johanna Nimmerfroh 1 Department of Biomedicine, University Hospital Basel and University of Basel, Switzerland; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Johanna%2BNimmerfroh%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Nimmerfroh%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJohanna%2BNimmerfroh%2B) Dinah Heiligensetzer 1 Department of Biomedicine, University Hospital Basel and University of Basel, Switzerland; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Dinah%2BHeiligensetzer%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Heiligensetzer%20D&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ADinah%2BHeiligensetzer%2B) Michael Thomas Sandholzer 2 University of Basel; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Luana%2BGuerra%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Guerra%20L&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ALuana%2BGuerra%2B) Heinz Läubli 2 University of Basel; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Heinz%2BL%C3%A4ubli%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=L%C3%A4ubli%20H&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AHeinz%2BL%25C3%25A4ubli%2B) * [ORCID record for Heinz Läubli](http://orcid.org/0000-0002-8910-5620 "Open in new tab") * For correspondence: heinz.laeubli@unibas.ch * [Abstract](https://www.biorxiv.org/content/10.64898/2026.08.02.742298v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5686154/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.08.02.742298v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5686154/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.08.02.742298v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5686154/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.08.02.742298v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5686154/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.08.02.742298v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5686154/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Aberrantly elevated cell-surface sialylation, or hypersialylation, is a common feature of human cancers and contributes to immune evasion. Sialidase-based therapies have therefore emerged as a strategy to disrupt this glyco-checkpoint. Although the immunosuppressive role of tumor-associated sialylation is well established, how sialylation on human T cells shapes anti-tumor responses remains poorly defined. Here, we identify surface sialoglycans on T cells, particularly alpha2,3-linked structures, as a cell-intrinsic restraint on human T cell activation, proliferation, and effector function. In vitro, enzymatic desialylation enhanced T cell activation, proliferation, cytokine production, and bispecific T cell engager (TCE)-mediated tumor-cell killing in healthy donor PBMC co-cultures. In ex vivo cultures of primary chronic lymphocytic leukemia (CLL) PBMCs, sialidase treatment combined with the CD20-directed TCE glofitamab enhanced cytotoxic effector transcriptional programming in autologous T cells. Single-cell RNA sequencing combined with lectin-based CITE-seq linked treatment-induced transcriptional states to lectin-defined cell-surface glycan signatures within the same single-cell dataset. This integrated analysis revealed that naive and, to a lesser extent, central memory T cells combined elevated baseline alpha2,3-sialylation signatures with the clearest transcriptional responses to glofitamab plus sialidase treatment. CD43 emerged as a major carrier of alpha2,3-linked sialoglycans, and its deletion attenuated sialidase-enhanced T cell activation. Together, these findings identify sialylation of the T cell surface as a subset-specific restraint on human TCE responses and provide a rationale for testing sialidase-TCE combinations designed to engage less-differentiated T cell populations. ### Competing Interest Statement M.B. reports grants from Novartis and personal fees from MSD, Roche Diagnostics, and Jazz Pharmaceuticals, outside the submitted work. H.L. reports grants from Ono Pharmaceuticals, Bristol Myers Squibb, GlycoEra, Palleon Pharmaceuticals, and Novartis and non-financial support from Glycocalyx Therapeutics, outside the submitted work. A. Zippelius received consulting and advisor fees from Bristol-Myers Squibb, Merck Sharp & Dohme, Hoffmann-La Roche, NBE Therapeutics, and Engimmune and maintains further noncommercial research agreements with Hoffmann-La Roche, T3 Pharma, Bright Peak Therapeutics, and AstraZeneca. The remaining authors declare no competing interests. ## Funder Information Declared ERC, 955575 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY-NC-ND 4.0 International license](http://creativecommons.org/licenses/by-nc-nd/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The
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