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Human T-Cell Leukemia Virus Type 1 (HTLV-1) p12^I Down-Modulates ICAM-1 and -2 and Reduces Adherence of Natural Killer Cells, 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 Infected Cells

Prabal Banerjee,¹ Gerold Feuer,^1, and Edward Barker^2*,

Department of Microbiology and Immunology SUNY Upstate Medical University, Syracuse, New York,¹ Department of Immunology and Microbiology, Rush University Medical Center, Chicago, Illinois²

Received 25 April 2007/ Accepted 26 June 2007

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 human T-cell leukemia virus type 1 (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 intercellular adhesion molecule 1 (ICAM-1) and ICAM-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 coactivating 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.

Published ahead of print on 3 July 2007.

G.F. and E.B. contributed equally to this study.

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