LFA-3 co-stimulates cytokine secretion by cytotoxic T lymphocytes by providing a TCR-independent activation signal

Eur J Immunol. 1998 Apr;28(4):1322-31. doi: 10.1002/(SICI)1521-4141(199804)28:04<1322::AID-IMMU1322>3.0.CO;2-I.

Abstract

T cell activation is known to depend not only on efficient antigen recognition and subsequent signaling through TCR, but also on interactions involving multiple adhesion and accessory molecules such as CD28/B7, LFA-1/ICAM-1 and LFA-3/CD2. The present study dissects the role of LFA-3/CD2 interactions in the activation of melanoma-specific CD8+ T cell clones. To this end we analyzed the influence of LFA-3 density on melanoma cells on lysis and cytokine production (TNF, IL-2, IFN-gamma) by T cells following activation by various amounts of antigenic peptides. Our results indicate that increasing LFA-3 density on melanoma cells variably affects their lysis susceptibility, but systematically and considerably enhances cytokine production by melanoma-specific cytotoxic T lymphocyte (CTL) clones. At any stimulatory antigen density, LFA-3 increased the fraction of responding cells and/or cytokine amounts produced by individual cells, without affecting TCR down-regulation. These results show that CD2 engagement increases cytokine gene activation essentially by providing to T cells a TCR-independent co-activation signal. From a practical point of view, our data demonstrate that the level of LFA-3 expressed on tumors critically affects cytokine production by specific CTL and thus the efficiency of specific immune reactions mediated by these cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD58 Antigens / immunology*
  • Cytokines / biosynthesis
  • Cytokines / immunology
  • Humans
  • Lymphocyte Activation / immunology*
  • Lymphocytes, Tumor-Infiltrating / immunology*
  • Melanoma / immunology*
  • Rats
  • Receptors, Antigen, T-Cell / immunology*
  • Signal Transduction / immunology
  • T-Lymphocytes, Cytotoxic / immunology*
  • Tumor Cells, Cultured

Substances

  • CD58 Antigens
  • Cytokines
  • Receptors, Antigen, T-Cell