Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffei

Abstract Background Macrophages are the first line of defense against Talaromyces marneffei. CD86 is a surface molecule expressed on antigen‐presenting cells, such as macrophages, that provide costimulatory signals necessary for T cell activation and survival. In a prior study, it was shown that as...

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Main Authors: Rifeng Chen, Di Yang, Linxia Shen, Jinling Fang, Raqib Khan, Donghua Liu
Format: Article
Language:English
Published: Wiley 2022-12-01
Series:Immunity, Inflammation and Disease
Subjects:
Online Access:https://doi.org/10.1002/iid3.740
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author Rifeng Chen
Di Yang
Linxia Shen
Jinling Fang
Raqib Khan
Donghua Liu
author_facet Rifeng Chen
Di Yang
Linxia Shen
Jinling Fang
Raqib Khan
Donghua Liu
author_sort Rifeng Chen
collection DOAJ
description Abstract Background Macrophages are the first line of defense against Talaromyces marneffei. CD86 is a surface molecule expressed on antigen‐presenting cells, such as macrophages, that provide costimulatory signals necessary for T cell activation and survival. In a prior study, it was shown that as infection progressed, CD86 expression levels in macrophages considerably declined while CD86 concentrations in the supernatant significantly increased. Additionally, M1 macrophage polarization was insufficient and switched to M2 macrophage polarization. Besides costimulation, however, additional roles of CD86 are not known or well‐studies. Therefore, we hypothesized that upregulating CD86 on macrophages might promote T. marneffei defense. Methods A lentivirus vector, called Lenti‐CD86, was used to infect THP‐1 cells to overexpress secretory CD86. Through killing assay, nitric oxide detection, and cytokine detection, the capacity of THP‐1 macrophages to phagocytose and kill T. marneffei was examined. Results In the current study, Lenti‐CD86 transfection of THP‐1 cells resulted in a signifant expression of CD86. Additionally, the THP‐1 macrophages stably transfected with Lenti‐CD86 showed higher nitric oxide and IL‐1β production, faster polarization, and stronger phagocytosis and killing capabilities than the non‐transfected or control virus transfected cells. Conclusion Our study shows that lentivirus‐mediated CD86 overexpression improves THP‐1 macrophages' capacity to phagocytose and eliminate T. marneffei.
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spelling doaj.art-0b0e6b0b61c94f5794a33592abf9b1da2022-12-22T04:16:48ZengWileyImmunity, Inflammation and Disease2050-45272022-12-011012n/an/a10.1002/iid3.740Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffeiRifeng Chen0Di Yang1Linxia Shen2Jinling Fang3Raqib Khan4Donghua Liu5Department of Dermatology The First Affiliated Hospital of Guangxi Medical University Nanning People's Republic of ChinaDepartment of Dermatology The First Affiliated Hospital of Guangxi Medical University Nanning People's Republic of ChinaDepartment of Dermatology The First Affiliated Hospital of Guangxi Medical University Nanning People's Republic of ChinaDepartment of Dermatology The First Affiliated Hospital of Guangxi Medical University Nanning People's Republic of ChinaDepartment of Dermatology The First Affiliated Hospital of Guangxi Medical University Nanning People's Republic of ChinaDepartment of Dermatology The First Affiliated Hospital of Guangxi Medical University Nanning People's Republic of ChinaAbstract Background Macrophages are the first line of defense against Talaromyces marneffei. CD86 is a surface molecule expressed on antigen‐presenting cells, such as macrophages, that provide costimulatory signals necessary for T cell activation and survival. In a prior study, it was shown that as infection progressed, CD86 expression levels in macrophages considerably declined while CD86 concentrations in the supernatant significantly increased. Additionally, M1 macrophage polarization was insufficient and switched to M2 macrophage polarization. Besides costimulation, however, additional roles of CD86 are not known or well‐studies. Therefore, we hypothesized that upregulating CD86 on macrophages might promote T. marneffei defense. Methods A lentivirus vector, called Lenti‐CD86, was used to infect THP‐1 cells to overexpress secretory CD86. Through killing assay, nitric oxide detection, and cytokine detection, the capacity of THP‐1 macrophages to phagocytose and kill T. marneffei was examined. Results In the current study, Lenti‐CD86 transfection of THP‐1 cells resulted in a signifant expression of CD86. Additionally, the THP‐1 macrophages stably transfected with Lenti‐CD86 showed higher nitric oxide and IL‐1β production, faster polarization, and stronger phagocytosis and killing capabilities than the non‐transfected or control virus transfected cells. Conclusion Our study shows that lentivirus‐mediated CD86 overexpression improves THP‐1 macrophages' capacity to phagocytose and eliminate T. marneffei.https://doi.org/10.1002/iid3.740CD86lentivirusoverexpressionTalaromyces marneffeiTHP‐1 macrophages
spellingShingle Rifeng Chen
Di Yang
Linxia Shen
Jinling Fang
Raqib Khan
Donghua Liu
Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffei
Immunity, Inflammation and Disease
CD86
lentivirus
overexpression
Talaromyces marneffei
THP‐1 macrophages
title Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffei
title_full Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffei
title_fullStr Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffei
title_full_unstemmed Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffei
title_short Overexpression of CD86 enhances the ability of THP‐1 macrophages to defend against Talaromyces marneffei
title_sort overexpression of cd86 enhances the ability of thp 1 macrophages to defend against talaromyces marneffei
topic CD86
lentivirus
overexpression
Talaromyces marneffei
THP‐1 macrophages
url https://doi.org/10.1002/iid3.740
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