Abstract
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.
Highlights
Despite being a minor population of myeloid cells, basophils play a vital role in the immune system [1,2,3,4]
Very few reports have delineated the expression of programmed death-ligand 1 (PD-L1) in basophils [6]
In this report, we determined the effect of IFN-γ on PD-L1 expression in human basophils
Summary
Despite being a minor population of myeloid cells, basophils play a vital role in the immune system [1,2,3,4]. Very few reports have delineated the expression of programmed death-ligand 1 (PD-L1) in basophils [6]. IFN-γ induces PD-L1 expression in human macrophages, neutrophils [12], and several cancer cells [13,14]. In this report, we determined the effect of IFN-γ on PD-L1 expression in human basophils. We found that IFN-γ induces PD-L1 expression in basophils. IFN-γ alone is insufficient to induce PD-L1 expression without IL-3 priming. Basophil priming is indispensable for IFN-γ-induced PD-L1 expression in basophils
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