Start Date
2022
Description
Th17 cells are found to be heavily depleted in the gut of HIV patients. Even after successful antiretroviral therapy, HIV patients exhibit a smaller Th17 population for years after treatment. Previous research has found human intestinal endothelial cells (IEC) to increase HIV infection of helper T cells. Using CCR6 as a marker for Th17, we investigated the effect of IEC on HIV infection of Th17 cells. IECs were found to increase the preferential infection of resting and activated CCR6+ cells. Th17 cells are known to be more susceptible to HIV infection than other types of CD4+ T cells. IEC stimulation increased the infection of all resting and activated CD4+ T cells, but had a greater effect on CCR6+ T helper cells. Moreover, coculturing CD4+ T cells with IEC reduced the proportion of CCR6+ T helper cells upon infection with HIV, suggesting that IECs facilitate preferential death of CCR6+ T cells. IEC’s role in CCR6+ T cell infection could be involved in the depletion of Th17 cells in HIV patients.
Recommended Citation
Pham, Fisher; Eddy, Jessica; Dapprich, Nathan; and Shen, Anding, "Preferential infection of CCR6+ CD4+ T Cells by HIV is increased by human intestinal endothelial cells" (2022). Summer Research. 31.
https://digitalcommons.calvin.edu/summer_research/2022/Posters/31
Included in
Preferential infection of CCR6+ CD4+ T Cells by HIV is increased by human intestinal endothelial cells
Th17 cells are found to be heavily depleted in the gut of HIV patients. Even after successful antiretroviral therapy, HIV patients exhibit a smaller Th17 population for years after treatment. Previous research has found human intestinal endothelial cells (IEC) to increase HIV infection of helper T cells. Using CCR6 as a marker for Th17, we investigated the effect of IEC on HIV infection of Th17 cells. IECs were found to increase the preferential infection of resting and activated CCR6+ cells. Th17 cells are known to be more susceptible to HIV infection than other types of CD4+ T cells. IEC stimulation increased the infection of all resting and activated CD4+ T cells, but had a greater effect on CCR6+ T helper cells. Moreover, coculturing CD4+ T cells with IEC reduced the proportion of CCR6+ T helper cells upon infection with HIV, suggesting that IECs facilitate preferential death of CCR6+ T cells. IEC’s role in CCR6+ T cell infection could be involved in the depletion of Th17 cells in HIV patients.
