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Journal of Virology, August 2002, p. 7528-7534, Vol. 76, No. 15
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.15.7528-7534.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Selective Loss of Innate CD4+ V{alpha}24 Natural Killer T Cells in Human Immunodeficiency Virus Infection

Johan K. Sandberg,1 Noam M. Fast,1 Emil H. Palacios,1 Glenn Fennelly,2 Joanna Dobroszycki,2 Paul Palumbo,3 Andrew Wiznia,2 Robert M. Grant,1 Nina Bhardwaj,4 Michael G. Rosenberg,2 and Douglas F. Nixon1*

Gladstone Institute of Virology and Immunology, University of California, San Francisco, California 94141,1 Jacobi Medical Center, Albert Einstein College of Medicine, Bronx, New York 10461,2 Department of Pediatrics, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 07103,3 The Rockefeller University, New York, New York 100214

Received 18 January 2002/ Accepted 22 April 2002

V{alpha}24 natural killer T (NKT) cells are innate immune cells involved in regulation of immune tolerance, autoimmunity, and tumor immunity. However, the effect of human immunodeficiency virus type 1 (HIV-1) infection on these cells is unknown. Here, we report that the V{alpha}24 NKT cells can be subdivided into CD4+ or CD4- subsets that differ in their expression of the homing receptors CD62L and CD11a. Furthermore, both CD4+ and CD4- NKT cells frequently express both CXCR4 and CCR5 HIV coreceptors. We find that the numbers of NKT cells are reduced in HIV-infected subjects with uncontrolled viremia and marked CD4+ T-cell depletion. The number of CD4+ NKT cells is inversely correlated with HIV load, indicating depletion of this subset. In contrast, CD4- NKT-cell numbers are unaffected in subjects with high viral loads. HIV infection experiments in vitro show preferential depletion of CD4+ NKT cells relative to regular CD4+ T cells, in particular with virus that uses the CCR5 coreceptor. Thus, HIV infection causes a selective loss of CD4+ lymph node homing (CD62L+) NKT cells, with consequent skewing of the NKT-cell compartment to a predominantly CD4- CD62L- phenotype. These data indicate that the key immunoregulatory NKT-cell compartment is compromised in HIV-1-infected patients.

* Corresponding author. Mailing address: Gladstone Institute of Virology and Immunology, University of California, P.O. Box 419100, San Francisco, CA 94141. Phone: (415) 695-3857. Fax: (415) 826-8449. E-mail: dnixon{at}gladstone.ucsf.edu.

Journal of Virology, August 2002, p. 7528-7534, Vol. 76, No. 15
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.15.7528-7534.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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