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J. Virol. doi:10.1128/JVI.00887-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

HTLV-1 p12^I down-modulates ICAM-1 and -2 and reduces natural killer cell adherence thereby protecting HTLV-1-infected primary CD4+ T cells from autologous natural killer cell-mediated cytotoxicity despite the reduction of major histocompatibility complex class I molecules on the infected cells

From: Department of Microbiology and Immunology SUNY Upstate Medical University, Syracuse, NY and; Department of Immunology and Microbiology, Rush University Medical Center, Chicago, IL

^* To whom correspondence should be addressed. Email: Edward_Barker{at}rush.edu.

	Abstract

Although, natural killer (NK) cell-mediated control of viral infections is well documented, very little is known about the ability of NK cells to restrain HTLV-1 infection. In the current study we show that NK cells are unable to kill HTLV-1-infected primary CD4+ T cells. Exposure of NK cells to interleukin-2 (IL-2) resulted in only a marginal increase in their ability to kill HTLV-1-infected primary CD4+ T cells. This inability of NK cells to kill HTLV-1-infected CD4+ T cells occurred despite the down-modulation of major histocompatibility complex (MHC) class I molecules, one of the ligands for the major NK cell inhibitory receptor, by HTLV-1 p12^I on CD4+ T cells. One reason for this diminished ability of NK cells to kill HTLV-1-infected cells was the decreased ability of NK cells to adhere to HTLV-1-infected cells because of HTLV-1 p12^I- mediated down-modulation of ICAM-1 and -2. We also found that HTLV-1-infected CD4+ T cells did not express ligands for NK cell activating receptors, NCR and NKG2D, although they did express ligands for NK cell co-activating receptors, NTB-A and 2B4. Thus, despite HTLV-1-mediated down-modulation of MHC-I molecules, HTLV-1-infected primary CD4+ T cells avoids NK cell destruction by modulating ICAM expression and shunning the expression of ligands for activating receptors.

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