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Terminal Effector CD8 T Cells Defined by an IKZF2⁺IL-7R^- Transcriptional Signature Express FcγRIIIA, Expand in HIV Infection, and Mediate Potent HIV-Specific Antibody-Dependent Cellular Cytotoxicity.

ABSTRACT: HIV-1 infection expands large populations of late-stage differentiated CD8 T cells that may persist long after viral escape from TCR recognition. In this study, we investigated whether such CD8 T cell populations can perform unconventional innate-like antiviral effector functions. Chronic untreated HIV-1 infection was associated with elevated numbers of CD45RA⁺CD57⁺ terminal effector CD8 T cells expressing FcγRIIIA (CD16). The FcγRIIIA⁺ CD8 T cells displayed a distinctive transcriptional profile between conventional CD8 T cells and NK cells, characterized by high levels of IKZF2 and low expression of IL7R This transcriptional profile translated into a distinct NKp80⁺ IL-7Rα^- surface phenotype with high expression of the H

SUBMITTER: Naluyima P

PROVIDER: S-EPMC6778306 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Dataset Information

Terminal Effector CD8 T Cells Defined by an IKZF2⁺IL-7R^- Transcriptional Signature Express FcγRIIIA, Expand in HIV Infection, and Mediate Potent HIV-Specific Antibody-Dependent Cellular Cytotoxicity.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Terminal Effector CD8 T Cells Defined by an IKZF2+IL-7R- Transcriptional Signature Express FcγRIIIA, Expand in HIV Infection, and Mediate Potent HIV-Specific Antibody-Dependent Cellular Cytotoxicity.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Terminal Effector CD8 T Cells Defined by an IKZF2⁺IL-7R^- Transcriptional Signature Express FcγRIIIA, Expand in HIV Infection, and Mediate Potent HIV-Specific Antibody-Dependent Cellular Cytotoxicity.