ArticleImmunity, inflammation and disease2022
Overexpression of CD86 enhances the ability of THP-1 macrophages to defend against Talaromyces marneffei.
Article in Immunity, inflammation and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 24 citations in OpenAlex.
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- Accelerating and protective effects toward cancer growth in cGAS and FcgRIIb deficient mice, respectively, an impact of macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Development and validation of a novel endoplasmic reticulum stress-related lncRNA signature in laryngeal squamous cell carcinoma.Scientific reports · 2025Article
- Development and in vitro evaluation of biomimetic injectable hydrogels from decellularized human nerves for central nervous system regeneration.Materials today. Bio · 2025Article
- CCN2 mediates fibroblast-macrophage interaction in knee arthrofibrosis based on single-cell RNA-seq analysis.Bone research · 2025Article
- Cell of origin alters myeloid-mediated immunosuppression in lung adenocarcinoma.bioRxiv : the preprint server for biology · 2024Article
- IL-8 Instructs Macrophage Identity in Lateral Ventricle Contacting Glioblastoma.bioRxiv : the preprint server for biology · 2024Article
- Article
- Overexpression of CD86 enhances the ability of THP-1 macrophages to defend against Talaromyces marneffei.Immunity, inflammation and disease · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMacrophages 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.
methodsA 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.
resultsIn 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.
conclusionOur study shows that lentivirus-mediated CD86 overexpression improves THP-1 macrophages' capacity to phagocytose and eliminate T. marneffei.
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