HLA class II molecules transduce accessory signals affecting the CD3 but not the interleukin-2 activation pathway in T blasts

Hum Immunol. 1993 Dec;38(4):251-60. doi: 10.1016/0198-8859(93)90552-c.

Abstract

MHC class II molecules play a central role in the control of the immune response, but their biologic function and mechanism of action on the surface of activated human T lymphocytes are not entirely understood. In our study, the functional role of HLA class II molecules in T-blast proliferation was investigated by analyzing in parallel the IL-2- and CD3-driven activation pathways. The results indicate that the cross-linking of class II and CD3 molecules significantly increased the CD3-mediated T-blast proliferation, while no effect was observed on the IL-2-driven cell activation. This phenomenon was not confined to either CD4+ or CD8+ subsets nor was specifically affected by CD45 triggering. Biochemical studies showed that signaling via MHC class II molecules in T blasts led to PKC membrane translocation and IP accumulation. The simultaneous triggering of CD3 and HLA class II molecules led to a synergistic effect on IP accumulation but did not increase the CD3-mediated PKC membrane translocation. Our data suggest that HLA class II molecules are involved in T-cell-T-cell interactions and can mediate accessory signals, affecting the T-lymphocyte activation state.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD3 Complex / physiology*
  • HLA-D Antigens / physiology*
  • Humans
  • Inositol Phosphates / blood
  • Interleukin-2 / physiology*
  • Lymphocyte Activation
  • Protein Kinase C / blood
  • Signal Transduction / physiology*
  • T-Lymphocyte Subsets / immunology*

Substances

  • CD3 Complex
  • HLA-D Antigens
  • Inositol Phosphates
  • Interleukin-2
  • Protein Kinase C