Asset Details
Do you wish to reserve the book?
M2-TAM subsets altered by lactic acid promote T-cell apoptosis through the PD-L1/PD-1 pathway
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
M2-TAM subsets altered by lactic acid promote T-cell apoptosis through the PD-L1/PD-1 pathway
Do you wish to request the book?
M2-TAM subsets altered by lactic acid promote T-cell apoptosis through the PD-L1/PD-1 pathway
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
M2-TAM subsets altered by lactic acid promote T-cell apoptosis through the PD-L1/PD-1 pathway
2020
Overview
The aim of the study was to investigate the effects of lactic acid on the phenotypic polarization and immune function of macrophages. The human monocyte/macrophage cell line, THP-1, was selected and treated with lactic acid. Immunofluorescence staining, laser confocal microscopy, reverse-transcription polymerase chain reaction (RT-PCR), western blot, siRNA, and ELISA analyses were used to observe changes in the levels of cluster of differentiation (CD)68, CD163, hypoxia inducible factor (HIF)-1α, and programmed death ligand-1 (PD-L1) as well as those of cytokines, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-12, and IL-10. THP-1 macrophages and T cells were co-cultured in vitro to observe the changes in proliferation and apoptosis of T cells. The results showed that, lactic acid (15 mmol/l) significantly upregulated the expression of the macrophage M2 marker CD163 (P<0.05), cytokines, IFN-γ and IL-10, secreted by M2-tumor-associated macrophages (TAM, P<0.05), and HIF-1α and PD-L1 (P<0.05), and downregulated the expression of cytokines, TNF-α and IL-12, secreted by M1-TAM (P<0.05). Redistribution of M2-TAM subsets and PD-L1 expression was reversed after further transfection of THP-1 cells with HIF-1α siRNA (P<0.05). After co-culturing, T-cell proliferation was inhibited and apoptosis was promoted. In summary, modulation of lactic acid level can redistribute M2-TAM subsets and upregulate PD-L1 to assist tumor immune escape. The HIF-1α signaling pathway may participate in this process, revealing that macrophages, as 'checkpoints' in organisms, are links that connect the immune status and tumor evolution, and can be used as a target in tumor treatment.
