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1. HIV-1-induced cytokines deplete homeostatic innate lymphoid cells and expand TCF7-dependent memory NK cells

Author

Wang, Yetao, Lifshitz, Lawrence, Gellatly, Kyle, Vinton, Carol L, Busman-Sahay, Kathleen, McCauley, Sean, Vangala, Pranitha, Kim, Kyusik, Derr, Alan, Jaiswal, Smita, Kucukural, Alper, McDonel, Patrick, Hunt, Peter W, Greenough, Thomas, Houghton, JeanMarie, Somsouk, Ma, Estes, Jacob D, Brenchley, Jason M, Garber, Manuel, Deeks, Steven G, and Luban, Jeremy

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, Infectious Diseases, Clinical Research, HIV/AIDS, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Infection, Good Health and Well Being, Cytokines, Gene Expression Regulation, HIV Infections, HIV-1, Homeostasis, Humans, Immunity, Innate, Immunologic Memory, In Vitro Techniques, Inflammation, Killer Cells, Natural, Lymphocytes, T Cell Transcription Factor 1, Wnt Signaling Pathway, Biochemistry and cell biology
Abstract

Human immunodeficiency virus 1 (HIV-1) infection is associated with heightened inflammation and excess risk of cardiovascular disease, cancer and other complications. These pathologies persist despite antiretroviral therapy. In two independent cohorts, we found that innate lymphoid cells (ILCs) were depleted in the blood and gut of people with HIV-1, even with effective antiretroviral therapy. ILC depletion was associated with neutrophil infiltration of the gut lamina propria, type 1 interferon activation, increased microbial translocation and natural killer (NK) cell skewing towards an inflammatory state, with chromatin structure and phenotype typical of WNT transcription factor TCF7-dependent memory T cells. Cytokines that are elevated during acute HIV-1 infection reproduced the ILC and NK cell abnormalities ex vivo. These results show that inflammatory cytokines associated with HIV-1 infection irreversibly disrupt ILCs. This results in loss of gut epithelial integrity, microbial translocation and memory NK cells with heightened inflammatory potential, and explains the chronic inflammation in people with HIV-1.

Published
2020

2. HIV-1-induced cytokines deplete homeostatic innate lymphoid cells and expand TCF7-dependent memory NK cells.

Author

Wang, Yetao, Lifshitz, Lawrence, Gellatly, Kyle, Vinton, Carol L, Busman-Sahay, Kathleen, McCauley, Sean, Vangala, Pranitha, Kim, Kyusik, Derr, Alan, Jaiswal, Smita, Kucukural, Alper, McDonel, Patrick, Hunt, Peter W, Greenough, Thomas, Houghton, JeanMarie, Somsouk, Ma, Estes, Jacob D, Brenchley, Jason M, Garber, Manuel, Deeks, Steven G, and Luban, Jeremy

Subjects
Lymphocytes, Killer Cells, Natural, Humans, HIV-1, HIV Infections, Inflammation, Cytokines, Immunologic Memory, Gene Expression Regulation, Homeostasis, T Cell Transcription Factor 1, Immunity, Innate, Wnt Signaling Pathway, In Vitro Techniques, Immunology
Abstract

Human immunodeficiency virus 1 (HIV-1) infection is associated with heightened inflammation and excess risk of cardiovascular disease, cancer and other complications. These pathologies persist despite antiretroviral therapy. In two independent cohorts, we found that innate lymphoid cells (ILCs) were depleted in the blood and gut of people with HIV-1, even with effective antiretroviral therapy. ILC depletion was associated with neutrophil infiltration of the gut lamina propria, type 1 interferon activation, increased microbial translocation and natural killer (NK) cell skewing towards an inflammatory state, with chromatin structure and phenotype typical of WNT transcription factor TCF7-dependent memory T cells. Cytokines that are elevated during acute HIV-1 infection reproduced the ILC and NK cell abnormalities ex vivo. These results show that inflammatory cytokines associated with HIV-1 infection irreversibly disrupt ILCs. This results in loss of gut epithelial integrity, microbial translocation and memory NK cells with heightened inflammatory potential, and explains the chronic inflammation in people with HIV-1.

Published
2020

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