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• W3126149671 abstract "Natural killer (NK) cells are innate cytolytic effectors that target HIV-infected CD4+ T cells. In conjunction with antibodies recognizing the HIV envelope, NK cells also eliminate HIV-infected targets through antibody-dependent cellular cytotoxicity (ADCC). However, how these NK cell functions impact infected macrophages is less understood. We show that HIV-infected macrophages resist NK cell-mediated killing. Compared with HIV-infected CD4+ T cells, initial innate NK cell interactions with HIV-infected macrophages skew the response toward cytokine production, rather than release of cytolytic contents, causing inefficient elimination of infected macrophages. Studies with chimeric antigen receptor (CAR) T cells demonstrate that the viral envelope is equally accessible on CD4+ T cells and macrophages. Nonetheless, ADCC against macrophages is muted compared with ADCC against CD4+ T cells. Thus, HIV-infected macrophages employ mechanisms to evade immediate cytolytic NK cell function while preserving inflammatory cytokine responses. These findings emphasize the importance of eliminating infected macrophages for HIV cure efforts." @default.
• W3126149671 created "2021-02-15" @default.
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• W3126149671 date "2021-03-01" @default.
• W3126149671 modified "2023-10-17" @default.
• W3126149671 title "HIV-infected macrophages resist efficient NK cell-mediated killing while preserving inflammatory cytokine responses" @default.
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• W3126149671 doi "https://doi.org/10.1016/j.chom.2021.01.006" @default.
• W3126149671 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8486985" @default.
• W3126149671 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33571449" @default.
• W3126149671 hasPublicationYear "2021" @default.
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