Distinct phenotype of unrestricted cytotoxic T lymphocytes from human immunodeficiency virus-infected individuals.

Abstract

INTRODUCTION:

Human immunodeficiency virus (HIV)-infected individuals have CD8(+) cytotoxic T lymphocytes (CTL) that kill activated uninfected T lymphocytes. These CTL are independent of class Ia human histocompatibility-linked leukocyte antigens (HLA-Ia).

METHODS:

To further characterize these CTL, we investigated their possible restriction to non-classical class Ib HLA-E molecules and their expression of natural killer cell receptors (NKR) that are often affected in HIV infection.

RESULTS:

We found no role for HLA-E in CTL-mediated killing of activated uninfected T lymphocytes. The non-HLA-restricted CTL did not express NKG2A, an inhibitory NKR that binds HLA-E, nor CD56, a prominent marker on previously described non-HLA-restricted CTL.

DISCUSSION:

This NKG2A(-)CD56(-) phenotype of HLA-unrestricted CTL that kill uninfected activated T lymphocytes matches generalized changes on CD8(+) T lymphocytes that occur in progressive HIV infection, suggesting these phenotypic changes may reflect pathogenic evolution of the CD8(+) T cell repertoire. These CTL represent a unique phenotypic and functional subset with potential relevance to HIV pathogenesis.

• Authors: Matthew S Parsons, Katrin Zipperlen, Maureen Gallant, Consie Howley, Michael Grant
• Journal: Journal of clinical immunology (J Clin Immunol) Vol. 30 Issue 2 Pg. 272-9 (Mar 2010) ISSN: 1573-2592 [Electronic] Netherlands
• PMID: 20099013 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antigens, CD
• HLA Antigens
• Receptors, Natural Killer Cell

Topics

• Antigens, CD (metabolism)
• Cell Separation
• Cells, Cultured
• Cytotoxicity, Immunologic
• Flow Cytometry
• HIV Infections (immunology, pathology)
• HIV-1 (immunology)
• HLA Antigens (metabolism)
• Humans
• Immunophenotyping
• Lymphocyte Activation
• Receptors, Natural Killer Cell (metabolism)
• T-Lymphocyte Subsets (immunology, metabolism, pathology, virology)
• T-Lymphocytes, Cytotoxic (immunology, metabolism, pathology, virology)