Use of the anti-inflammatory cytokine interleukin-11 to reverse HIV-1gp120 repression of a natural killer cell line.
Enhancing natural killer (NK) cell activation has been associated with protection from human immunodeficiency virus-1 (HIV-1) infections and slowed onset of immunodeficiency. However, soluble HIV-1 envelope protein, gp120, has been shown to impair NK cell cytokine secretion and cell-mediated cytotoxicity. Here we show that gp120 suppressed IFN-γ production and cytotoxic function of a human NK cell line NK-92MI. We furthermore demonstrated that an anti-inflammatory cytokine interleukin-11 can restore effector functions to repressed NK-92MI cells. These studies support the notion that IL-11 administration may reduce HIV-1-mediated immune activation and exhaustion while achieving elimination of virally-infected cells through restored NK cell function.
Department of Basic Sciences, Georgia Campus, Philadelphia College of Osteopathic Medicine, Suwanee, GA 30024, USA.
Sheena E
SE
Favors
Lindsay M
LM
Curd
Randal K
RK
Gregg
D002460:Cell Line; D003602:Cytotoxicity, Immunologic; D015699:HIV Envelope Protein gp120 / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D017370:Interleukin-11 / Q000276:immunology*; D007694:Killer Cells, Natural / Q000276:immunology*
D015699:HIV Envelope Protein gp120; D017370:Interleukin-11; C514793:gp120 protein, Human immunodeficiency virus 1; D007371:Interferon-gamma