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IFN-γ Induces PD-L1 Expression in Primed Human Basophils

Programmed death-ligand 1 (PD-L1) plays a key role in maintaining immune tolerance and also in immune evasion of cancers and pathogens. Though the identity of stimuli that induce PD-L1 in various human innate cells and their function are relatively well studied, data on the basophils remain scarce....

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Autores principales: Bonam, Srinivasa Reddy, Chauvin, Camille, Mathew, Mano J., Bayry, Jagadeesh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8909048/
https://www.ncbi.nlm.nih.gov/pubmed/35269423
http://dx.doi.org/10.3390/cells11050801
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author Bonam, Srinivasa Reddy
Chauvin, Camille
Mathew, Mano J.
Bayry, Jagadeesh
author_facet Bonam, Srinivasa Reddy
Chauvin, Camille
Mathew, Mano J.
Bayry, Jagadeesh
author_sort Bonam, Srinivasa Reddy
collection PubMed
description Programmed death-ligand 1 (PD-L1) plays a key role in maintaining immune tolerance and also in immune evasion of cancers and pathogens. Though the identity of stimuli that induce PD-L1 in various human innate cells and their function are relatively well studied, data on the basophils remain scarce. In this study, we have identified one of the factors, such as IFN-γ, that induces PD-L1 expression in human basophils. Interestingly, we found that basophil priming by IL-3 is indispensable for IFN-γ-induced PD-L1 expression in human basophils. However, priming by other cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF) and thymic stromal lymphopoietin (TSLP) was dispensable. Analyses of a published microarray data set on IL-3-treated basophils indicated that IL-3 enhances IFNGR2, one of the chains of the IFNGR heterodimer complex, and CD274, thus providing a mechanistic insight into the role of IL-3 priming in IFN-γ-induced PD-L1 expression in human basophils.
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spelling pubmed-89090482022-03-11 IFN-γ Induces PD-L1 Expression in Primed Human Basophils Bonam, Srinivasa Reddy Chauvin, Camille Mathew, Mano J. Bayry, Jagadeesh Cells Article Programmed death-ligand 1 (PD-L1) plays a key role in maintaining immune tolerance and also in immune evasion of cancers and pathogens. Though the identity of stimuli that induce PD-L1 in various human innate cells and their function are relatively well studied, data on the basophils remain scarce. In this study, we have identified one of the factors, such as IFN-γ, that induces PD-L1 expression in human basophils. Interestingly, we found that basophil priming by IL-3 is indispensable for IFN-γ-induced PD-L1 expression in human basophils. However, priming by other cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF) and thymic stromal lymphopoietin (TSLP) was dispensable. Analyses of a published microarray data set on IL-3-treated basophils indicated that IL-3 enhances IFNGR2, one of the chains of the IFNGR heterodimer complex, and CD274, thus providing a mechanistic insight into the role of IL-3 priming in IFN-γ-induced PD-L1 expression in human basophils. MDPI 2022-02-25 /pmc/articles/PMC8909048/ /pubmed/35269423 http://dx.doi.org/10.3390/cells11050801 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Bonam, Srinivasa Reddy
Chauvin, Camille
Mathew, Mano J.
Bayry, Jagadeesh
IFN-γ Induces PD-L1 Expression in Primed Human Basophils
title IFN-γ Induces PD-L1 Expression in Primed Human Basophils
title_full IFN-γ Induces PD-L1 Expression in Primed Human Basophils
title_fullStr IFN-γ Induces PD-L1 Expression in Primed Human Basophils
title_full_unstemmed IFN-γ Induces PD-L1 Expression in Primed Human Basophils
title_short IFN-γ Induces PD-L1 Expression in Primed Human Basophils
title_sort ifn-γ induces pd-l1 expression in primed human basophils
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8909048/
https://www.ncbi.nlm.nih.gov/pubmed/35269423
http://dx.doi.org/10.3390/cells11050801
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