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<h4>Background</h4>Natural killer (NK) cells are an important type of effector cell in the innate immune response, and also have a role in regulation of the adaptive immune response. Several studies have indicated that NK cells may influence CD4+ T cells during HIV infection.<h4>Methods</h4>In total, 51 HIV-infected individuals and 15 healthy controls participated in this study. We performed the flow cytometry assays and real-time PCR for the phenotypic analysis and the functional assays of NK cell-mediated deletion of CD4+ T cells, phosphorylation of nuclear factor-κB (NF-κB/p65) and the intervention of metformin.<h4>Results</h4>Here we detected high CD54 expression on CD4+ T cells in HIV-infected individuals, and demonstrate that upregulated CD54 is associated with disease progression in individuals infected with HIV. We also show that CD54 expression leads to the deletion of CD4+ T cells by NK cells in vitro, and that this is modulated by NF-κB/p65 signaling. Further, we demonstrate that metformin can suppress CD54 expression on CD4+ T cells by inhibiting NF-κB/p65 phosphorylation.<h4>Conclusions</h4>Our data suggest that further studies to evaluate the potential role of metformin as adjunctive therapy to reconstitute immune function in HIV-infected individuals are warranted.

Original publication




Journal article


The Journal of infectious diseases

Publication Date





1892 - 1903


NHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine.


Killer Cells, Natural, CD4-Positive T-Lymphocytes, Humans, HIV-1, HIV Infections, Disease Progression, Metformin, NF-kappa B, Intercellular Adhesion Molecule-1, CD4 Lymphocyte Count, Viral Load, Immunophenotyping, Lymphocyte Activation, Cell Communication, Cytotoxicity, Immunologic, Gene Expression, Phosphorylation, Adult, Female, Male, Host-Pathogen Interactions, Young Adult