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HIV-1 broadly neutralizing antibodies (bnAbs) are difficult to induce with vaccines but are generated in ∼50% of HIV-1-infected individuals. Understanding the molecular mechanisms of host control of bnAb induction is critical to vaccine design. Here, we performed a transcriptome analysis of blood mononuclear cells from 47 HIV-1-infected individuals who made bnAbs and 46 HIV-1-infected individuals who did not and identified in bnAb individuals upregulation of RAB11FIP5, encoding a Rab effector protein associated with recycling endosomes. Natural killer (NK) cells had the highest differential expression of RAB11FIP5, which was associated with greater dysregulation of NK cell subsets in bnAb subjects. NK cells from bnAb individuals had a more adaptive/dysfunctional phenotype and exhibited impaired degranulation and cytokine production that correlated with RAB11FIP5 transcript levels. Moreover, RAB11FIP5 overexpression modulated the function of NK cells. These data suggest that NK cells and Rab11 recycling endosomal transport are involved in regulation of HIV-1 bnAb development.

Original publication

DOI

10.1016/j.cell.2018.08.064

Type

Journal article

Journal

Cell

Publication Date

10/2018

Volume

175

Pages

387 - 399.e17

Addresses

Duke Human Vaccine Institute, Duke University School of Medicine, Durham, NC 27710, USA; Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: todd.bradley@duke.edu.

Keywords

B-Lymphocytes, Killer Cells, Natural, Cell Line, Humans, HIV-1, HIV Infections, Adaptor Proteins, Signal Transducing, AIDS Vaccines, HIV Antibodies, Cohort Studies, Gene Expression Profiling, Adult, Middle Aged, Female, Male, Antibodies, Neutralizing