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.
Conclusion
Our study shows that lentivirus-mediated CD86 overexpression improves THP-1 macrophages' capacity to phagocytose and eliminate T. marneffei.
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.