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Infection and depletion of CD4+ group-1 innate lymphoid cells by HIV-1 via type-I interferon pathway.

Infection and depletion of CD4+ group-1 innate lymphoid cells by HIV-1 via type-I interferon pathway.
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Zhao J, Cheng L, Wang H, Yu H, Tu B, Fu Q, Li G, Wang Q, Sun Y, Zhang X, Liu Z, Chen W, Zhang L, Su L, Zhang Z,


Zhao J, Cheng L, Wang H, Yu H, Tu B, Fu Q, Li G, Wang Q, Sun Y, Zhang X, Liu Z, Chen W, Zhang L, Su L, Zhang Z, (click to view)

Zhao J, Cheng L, Wang H, Yu H, Tu B, Fu Q, Li G, Wang Q, Sun Y, Zhang X, Liu Z, Chen W, Zhang L, Su L, Zhang Z,

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PLoS pathogens 2018 01 0514(1) e1006819 doi 10.1371/journal.ppat.1006819
Abstract

Innate lymphoid cells (ILCs) are severely depleted during chronic HIV-1 infection by unclear mechanisms. We report here that human ILC1s comprising of CD4+ and CD4- subpopulations were present in various human lymphoid organs but with different transcription programs and functions. Importantly, CD4+ ILC1s expressed HIV-1 co-receptors and were productively infected by HIV-1 in vitro and in vivo. Furthermore, chronic HIV-1 infection activated and depleted both CD4+ and CD4- ILC1s, and impaired their cytokine production activity. Highly active antiretroviral (HAART) therapy in HIV-1 patients efficiently rescued the ILC1 numbers and reduced their activation, but failed to restore their functionality. We also found that blocking type-I interferon (IFN-I) signaling during HIV-1 infection in vivo in humanized mice prevented HIV-1 induced depletion or apoptosis of ILC1 cells. Therefore, we have identified the CD4+ ILC1 cells as a new target population for HIV-1 infection, and revealed that IFN-I contributes to the depletion of ILC1s during HIV-1 infection.

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