Anti-T cell receptor antibodies fail to inhibit specific lysis by CTL clones but activate lytic activity for irrelevant targets.
Open Access
- 15 February 1987
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 138 (4) , 1221-1228
- https://doi.org/10.4049/jimmunol.138.4.1221
Abstract
In this report, we describe the functional effects of anti-T cell receptor antibodies on a panel of MHC-restricted, influenza virus-specific CTL clones. Approximately 25 to 30% of these clones are recognized by KJ16-133, an anti-T cell receptor monoclonal antibody presumably specific for products of the V beta 8 gene family, and an antibody with similar specificity, F23.1. In contrast to most previous reports, both KJ16-133 and F23.1, over a wide range of antibody concentrations, fail to inhibit the antigen-specific effector function of these CTL. Instead, the antibodies activate the CTL to kill without regard for the MHC haplotype of the target cells or the presence of the appropriate viral antigen. This anti-T cell receptor antibody-induced cytolysis by our clones does not appear to be mediated by Fc receptors on target cells. Nuclear destruction of target cells as a result of antibody-induced lysis suggests that it occurs via a mechanism similar to antigen-specific lysis by CTL. In addition, both soluble bivalent F23.1 and F23.1 coupled-Sepharose beads are able to induce the secretion of interferon-gamma from these CTL clones.This publication has 3 references indexed in Scilit:
- Fine specificity and antigen receptor expression among influenza virus-specific cytolytic T lymphocyte clones.The Journal of Immunology, 1986
- The major histocompatibility complex-restricted antigen receptor on T cells. I. Isolation with a monoclonal antibody.The Journal of Experimental Medicine, 1983
- Mechanisms of immune lysis. I. Physiological distinction between target cell death mediated by cytotoxic T lymphocytes and antibody plus complement.The Journal of Immunology, 1980