VSTM1-v2 does not drive human Th17 cell differentiation: A replication study

Helen J von Richthofen; Florianne M J Hafkamp; Anouk van Haperen; Esther C de Jong; Linde Meyaard

doi:10.1371/journal.pone.0284404

VSTM1-v2 does not drive human Th17 cell differentiation: A replication study

PLoS One. 2023 Apr 13;18(4):e0284404. doi: 10.1371/journal.pone.0284404. eCollection 2023.

Authors

Helen J von Richthofen^{1

2}, Florianne M J Hafkamp³, Anouk van Haperen^{1

2}, Esther C de Jong³, Linde Meyaard^{1

2}

Affiliations

¹ Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
² Oncode Institute, Utrecht, The Netherlands.
³ Department of Experimental Immunology, Amsterdam Institute for Infection & Immunity, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Abstract

Signal inhibitory receptor on leukocytes-1 (SIRL-1) is an immune inhibitory receptor expressed on human myeloid cells. We previously showed that dendritic cell (DC)-driven Th17 cell differentiation of human naive CD4+ T cells requires presence of neutrophils, which is inhibited by SIRL-1 ligation. VSTM1-v2 is a soluble isoform of SIRL-1, which was previously proposed to function as a Th17 polarizing cytokine. Here, we investigated the effect of VSTM1-v2 on DC-driven Th17 cell development. Neutrophils induced DC-driven Th17 cell differentiation, which was not enhanced by VSTM1-v2. Similarly, we found no effect of VSTM1-v2 on cytokine-driven Th17 cell development. Thus, our results do not support a role for VSTM1-v2 in Th17 cell differentiation.

Copyright: © 2023 von Richthofen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Cell Differentiation
Cytokines*
Dendritic Cells
Humans
Neutrophils
Protein Isoforms
Th17 Cells*

Substances

Cytokines
Protein Isoforms
VSTM1 protein, human

Grants and funding

This work was supported by Amsterdam UMC, University of Amsterdam, and by a Vici grant from the Netherlands Organization for Scientific Research (NWO, grant no. 91815608, www.nwo.nl). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.