HIV‐1 Nef impairs the dynamic of DC/NK crosstalk: different outcome of CD56dimand CD56brightNK cell subsets

Crosstalk
DOI: 10.1096/fj.06-7883com Publication Date: 2007-04-13T00:40:33Z
ABSTRACT
Dendritic cells (DCs) and natural killer (NK) are essential components of the innate immunity play a critical role in first phase host defense against infection. Interactions between DCs NK have been demonstrated variety settings, with evidence emerging complex bidirectional crosstalk two cell types. The accessory HIV-1 Nef protein is crucial determinant for viral replication pathogenesis. We previously that Nef, hijacking DC functional activity, subverts arm immune response to escape adaptive attack. Here, we monitor effect on outcome response, focusing impact DC/NK crosstalk. demonstrate up-regulates ability stimulate immunoregulatory (CD56(bright)) as assessed by activated phenotype, up-regulation their proliferative INF-gamma release. On other hand, Nef-pulsed inhibit cytotoxic (CD56(dim)), reduced HLA-DR surface expression, proliferation activity. Moreover, presence DCs, found significant TNF-alpha secretion reduction IL-10, GM-CSF, MIP-1alpha RANTES secretion. Our findings suggest Nef-induced dysregulation may represent potential mechanism through which HIV escapes surveillance.
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