|
|
||||||||
The Journal of Immunology, Vol 131, Issue 5 2296-2300, Copyright © 1983 by American Association of Immunologists
ARTICLES |
NK Damle, N Mohagheghpour, JA Hansen and EG Engleman
Although Leu-2+ (OKT8+) T cells activated in the mixed lymphocyte reaction (MLR) mediate both alloantigen-specific cytotoxicity and suppression of alloantigen-induced proliferation, it is not known whether these functions derive from a single cell type or phenotypically distinct cells. This study was undertaken to examine the alloantigen-specific cytolytic and suppressor potential of two subpopulations of Leu-2+ cells distinguishable from one another on the basis of their binding to the monoclonal antibody 9.3. Leu-2+, 9.3+ and Leu-2+, 9.3- populations were purified from peripheral blood, cultured for 7 days with autologous helper/inducer (Leu-3+) cells and allogeneic non-T cells, and reisolated before testing for cytotoxicity and suppression. All detectable alloantigen-specific cytolytic activity was confined to the Leu-2+, 9.3+ subpopulation. Killing by this subset was specific for the HLA-A and B (class I) major histocompatibility complex (MHC) antigens of the priming cell. By contrast, suppression of proliferation was mediated predominantly by the Leu-2+, 9.3- cells, and suppression by this subpopulation was specific for the HLA-DR (class II) MHC antigens of the priming cell. The development of suppression by Leu-2+, 9.3- cells was unaffected by cyclosporin A (CsA), an agent shown previously to block the development of cytolytic but not suppressor cells in MLR. Alloactivated Leu-2+, 9.3+ cells were slightly inhibitory of fresh MLR, but this effect as well as the development of cytolytic cells was completely abrogated by CsA. These results indicate that suppressor and cytolytic Leu-2+ T cells activated in MLR are derived from distinct precursors separable by antibody 9.3.
This article has been cited by other articles:
![]() |
A. Canton, E. M. Martinez-Caceres, C. Hernandez, C. Espejo, J. Garcia-Arumi, and R. Simo CD4-CD8 and CD28 Expression in T Cells Infiltrating the Vitreous Fluid in Patients With Proliferative Diabetic Retinopathy: A Flow Cytometric Analysis Arch Ophthalmol, May 1, 2004; 122(5): 743 - 749. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. D. Sempowski, S. J. Cross, C. S. Heinly, R. M. Scearce, and B. F. Haynes CD7 and CD28 Are Required for Murine CD4+CD25+ Regulatory T Cell Homeostasis and Prevention of Thyroiditis J. Immunol., January 15, 2004; 172(2): 787 - 794. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. S. Heinly, G. D. Sempowski, D. M. Lee, D. D. Patel, P. M. McDermott, R. M. Scearce, C. B. Thompson, and B. F. Haynes Comparison of thymocyte development and cytokine production in CD7-deficient, CD28-deficient and CD7/CD28 double-deficient mice Int. Immunol., February 1, 2001; 13(2): 157 - 166. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Anumanthan, A. Bensussan, L. Boumsell, A. D. Christ, R. S. Blumberg, S. D. Voss, A. T. Patel, M. J. Robertson, L. M. Nadler, and G. J. Freeman Cloning of BY55, a Novel Ig Superfamily Member Expressed on NK Cells, CTL, and Intestinal Intraepithelial Lymphocytes J. Immunol., September 15, 1998; 161(6): 2780 - 2790. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |