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Gaiha, Gaurav D.; McKim, Kevin J.; Woods, Matthew; Pertel, Thomas; Rohrbach, Janine; Barteneva, Natasha; Chin, Christopher R.; Liu, Dongfang; Soghoian, Damien Z.; Cesa, Kevin; Wilton, Shannon; Waring, Michael T.; Chicoine, Adam; Doering, Travis; Wherry, E. John; Kaufmann, Daniel E.; Lichterfeld, Mathias; Brass, Abraham L.; Walker, Bruce D.
Immunity, 12/2014, Letnik: 41, Številka: 6Journal Article
Decreased HIV-specific CD8+ T cell proliferation is a hallmark of chronic infection, but the mechanisms of decline are unclear. We analyzed gene expression profiles from antigen-stimulated HIV-specific CD8+ T cells from patients with controlled and uncontrolled infection and identified caspase-8 as a correlate of dysfunctional CD8+ T cell proliferation. Caspase-8 activity was upregulated in HIV-specific CD8+ T cells from progressors and correlated positively with disease progression and programmed cell death-1 (PD-1) expression, but negatively with proliferation. In addition, progressor cells displayed a decreased ability to upregulate membrane-associated caspase-8 activity and increased necrotic cell death following antigenic stimulation, implicating the programmed cell death pathway necroptosis. In vitro necroptosis blockade rescued HIV-specific CD8+ T cell proliferation in progressors, as did silencing of necroptosis mediator RIPK3. Thus, chronic stimulation leading to upregulated caspase-8 activity contributes to dysfunctional HIV-specific CD8+ T cell proliferation through activation of necroptosis and increased cell death. •HIV-specific CD8+ T cells from progressors have upregulated caspase-8 activity•Increased caspase-8 activity correlates with impaired proliferative capacity•Stimulation of progressor HIV-specific CD8+ T cells results in necrotic cell death•Blockade of necroptosis rescues progressor HIV-specific CD8+ T cell proliferation Decreased HIV-specific CD8+ T cell proliferation is a hallmark of chronic infection. Walker and colleagues identify necroptosis as a key cellular pathway that limits effective CD8+ T cell expansion during chronic HIV infection.
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