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

Autor: Zhao J; Research Center for Clinical & Translational Medicine, Beijing 302 Hospital, Beijing China., Cheng L; The Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America., Wang H; Research Center for Liver Transplantation, Beijing 302 Hospital, Beijing, China., Yu H; The Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America.; Key laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Science, Beijing, China., Tu B; Department of Infectious Diseases, Beijing 302 Hospital, Beijing, China., Fu Q; The Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America.; Department of Immonology, Binzhou Medical University, Yantai, Shandong, China., Li G; The Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America., Wang Q; The Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America., Sun Y; Research Center for Liver Transplantation, Beijing 302 Hospital, Beijing, China., Zhang X; Department of Infectious Diseases, Beijing 302 Hospital, Beijing, China., Liu Z; Research Center for Liver Transplantation, Beijing 302 Hospital, Beijing, China., Chen W; Department of Infectious Diseases, Beijing 302 Hospital, Beijing, China., Zhang L; Key laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Science, Beijing, China., Su L; The Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America.; Key laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Science, Beijing, China., Zhang Z; Research Center for Clinical & Translational Medicine, Beijing 302 Hospital, Beijing China.; The Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, United States of America.
Jazyk: angličtina
Zdroj: PLoS pathogens [PLoS Pathog] 2018 Jan 05; Vol. 14 (1), pp. e1006819. Date of Electronic Publication: 2018 Jan 05 (Print Publication: 2018).
DOI: 10.1371/journal.ppat.1006819
Abstrakt: 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.
Databáze: MEDLINE
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