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Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation

The dendritic cell (DC)-derived cytokine profile contributes to naive T cell differentiation, thereby directing the immune response. IL-37 is a cytokine with anti-inflammatory characteristics that has been demonstrated to induce tolerogenic properties in DC. In this study we aimed to evaluate the in...

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Autores principales: Kouwenberg, M., Pulskens, W. P. C., Diepeveen, L., Bakker-van Bebber, M., Dinarello, C. A., Netea, M. G., Hilbrands, L. B., van der Vlag, J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8143410/
https://www.ncbi.nlm.nih.gov/pubmed/34029331
http://dx.doi.org/10.1371/journal.pone.0251809
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author Kouwenberg, M.
Pulskens, W. P. C.
Diepeveen, L.
Bakker-van Bebber, M.
Dinarello, C. A.
Netea, M. G.
Hilbrands, L. B.
van der Vlag, J.
author_facet Kouwenberg, M.
Pulskens, W. P. C.
Diepeveen, L.
Bakker-van Bebber, M.
Dinarello, C. A.
Netea, M. G.
Hilbrands, L. B.
van der Vlag, J.
author_sort Kouwenberg, M.
collection PubMed
description The dendritic cell (DC)-derived cytokine profile contributes to naive T cell differentiation, thereby directing the immune response. IL-37 is a cytokine with anti-inflammatory characteristics that has been demonstrated to induce tolerogenic properties in DC. In this study we aimed to evaluate the influence of IL-37 on DC–T cell interaction, with a special focus on the role of the chemokine CXCL1. DC were cultured from bone marrow of human IL-37 transgenic (hIL-37Tg) or WT mice. The phenotype of unstimulated and LPS-stimulated DC was analyzed (co-stimulatory molecules and MHCII by flow cytometry, cytokine profile by RT-PCR and ELISA), and T cell stimulatory capacity was assessed in mixed lymphocyte reaction. The role of CXCL1 in T cell activation was analyzed in T cell stimulation assays with anti-CD3 or allogeneic DC. The expression of the co-stimulatory molecules CD40, CD80 and CD86, and of MHCII in LPS-stimulated DC was not affected by endogenous expression of IL-37, whereas LPS-stimulated hIL-37Tg DC produced less CXCL1 compared to LPS-stimulated WT DC. T cell stimulatory capacity of LPS-matured hIL-37Tg DC was comparable to that of WT DC. Recombinant mouse CXCL1 did not increase T cell proliferation either alone or in combination with anti-CD3 or allogeneic DC, nor did CXCL1 affect the T cell production of interferon-γ and IL-17. Endogenous IL-37 expression does not affect mouse DC phenotype or subsequent T cell stimulatory capacity, despite a reduced CXCL1 production. In addition, we did not observe an effect of CXCL1 in T cell proliferation or differentiation.
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spelling pubmed-81434102021-06-07 Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation Kouwenberg, M. Pulskens, W. P. C. Diepeveen, L. Bakker-van Bebber, M. Dinarello, C. A. Netea, M. G. Hilbrands, L. B. van der Vlag, J. PLoS One Research Article The dendritic cell (DC)-derived cytokine profile contributes to naive T cell differentiation, thereby directing the immune response. IL-37 is a cytokine with anti-inflammatory characteristics that has been demonstrated to induce tolerogenic properties in DC. In this study we aimed to evaluate the influence of IL-37 on DC–T cell interaction, with a special focus on the role of the chemokine CXCL1. DC were cultured from bone marrow of human IL-37 transgenic (hIL-37Tg) or WT mice. The phenotype of unstimulated and LPS-stimulated DC was analyzed (co-stimulatory molecules and MHCII by flow cytometry, cytokine profile by RT-PCR and ELISA), and T cell stimulatory capacity was assessed in mixed lymphocyte reaction. The role of CXCL1 in T cell activation was analyzed in T cell stimulation assays with anti-CD3 or allogeneic DC. The expression of the co-stimulatory molecules CD40, CD80 and CD86, and of MHCII in LPS-stimulated DC was not affected by endogenous expression of IL-37, whereas LPS-stimulated hIL-37Tg DC produced less CXCL1 compared to LPS-stimulated WT DC. T cell stimulatory capacity of LPS-matured hIL-37Tg DC was comparable to that of WT DC. Recombinant mouse CXCL1 did not increase T cell proliferation either alone or in combination with anti-CD3 or allogeneic DC, nor did CXCL1 affect the T cell production of interferon-γ and IL-17. Endogenous IL-37 expression does not affect mouse DC phenotype or subsequent T cell stimulatory capacity, despite a reduced CXCL1 production. In addition, we did not observe an effect of CXCL1 in T cell proliferation or differentiation. Public Library of Science 2021-05-24 /pmc/articles/PMC8143410/ /pubmed/34029331 http://dx.doi.org/10.1371/journal.pone.0251809 Text en © 2021 Kouwenberg et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Kouwenberg, M.
Pulskens, W. P. C.
Diepeveen, L.
Bakker-van Bebber, M.
Dinarello, C. A.
Netea, M. G.
Hilbrands, L. B.
van der Vlag, J.
Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation
title Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation
title_full Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation
title_fullStr Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation
title_full_unstemmed Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation
title_short Reduced CXCL1 production by endogenous IL-37 expressing dendritic cells does not affect T cell activation
title_sort reduced cxcl1 production by endogenous il-37 expressing dendritic cells does not affect t cell activation
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8143410/
https://www.ncbi.nlm.nih.gov/pubmed/34029331
http://dx.doi.org/10.1371/journal.pone.0251809
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