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Blood, 15 August 2007, Vol. 110, No. 4, pp. 1207-1214.
Prepublished online as a Blood First Edition Paper on May 18, 2007; DOI 10.1182/blood-2006-06-028175.
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IMMUNOBIOLOGY
HIV modulates the expression of ligands important in triggering natural killer cell cytotoxic responses on infected primary T-cell blasts
Jeffrey Ward1,
Matthew Bonaparte1,
Jennifer Sacks1,
Jacqueline Guterman1,
Manuela Fogli2,
Domenico Mavilio2, and
Edward Barker3
1 Department of Microbiology and Immunology, State University of New York, Upstate Medical University, Syracuse, NY;
2 Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD;
3 Department of Immunology and Microbiology, Rush University Medical Center, Chicago, IL
The ability of natural killer (NK) cells to kill virus-infected cells depends on the presence of ligands for activation receptors on the target cells. We found the presence of few, if any, NKp30 and NK46 ligands on T cell blasts infected with HIV, although NKp44 ligands were found on infected cells. HIV does induce the NKG2D ligands ULBP-1, -2, and -3. These ligands are involved in triggering NK cells to kill autologous HIV-infected cells, because interfering with the interaction between NKG2D, but not NKp46, on NK cells and its ligands on HIV-infected cells drastically reduced the lysis of infected cells. Interfering with the binding of the NK-cell coreceptors NTB-A and 2B4 to their ligands also decreased destruction by NK cells. The coreceptor ligands, NTB-A and CD48, were also found to be down-regulated during the course of HIV infection. Thus, ligands for NK-cell receptors are modulated during the course of HIV infection, which may greatly alter NK cells' ability to kill the infected cells.
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