L3T4 but not LFA-1 participates in antigen presentation by Ak-positive L-cell transformants

Immunogenetics. 1985;22(3):247-56. doi: 10.1007/BF00404484.


We report that mouse L cells expressing Ak class II molecules on their surface after DNA-mediated gene transfer are capable of presenting the synthetic copolymer (Glu60 Ala30 Tyr10) to Ak-restricted long-term T-cell clones. Antigen-induced T-cell stimulation could be inhibited by monoclonal antibodies (mAb) directed at spatially distinct determinants of the alpha and/or beta subunits of the Ak molecule, and by the rat L3T4-specific mAb H129.19. In contrast, several rat mAb reactive with the mouse LFA-1 molecule failed to inhibit T-cell activation when L cells were used as antigen-presenting cells (APC), although these mAb strongly inhibited the same T-cell responses in the presence of leukocytic APC. Similarly, the cytolytic activity of the Ak-specific T-cell clone A15.1.17 was blocked by L3T4-specific and by LFA-1-specific mAb when tested on Ak-positive B-cell hybridomas, but only by L3T4-specific mAb and not by LFA-1-specific mAb when Ak-positive L-cell transformants were used as targets. These data support the notion that the LFA-1 molecule is not necessary for T-cell activation, and suggest that its functional role as an accessory molecule depends on the leukocytic nature of the APC tested.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • Antibody Specificity
  • Antigen-Presenting Cells / immunology*
  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Surface / immunology*
  • Histocompatibility Antigens Class II / immunology*
  • L Cells
  • Macromolecular Substances
  • Mice
  • Peptides / immunology
  • Polymers
  • T-Lymphocytes / immunology*
  • T-Lymphocytes, Helper-Inducer / immunology*
  • Transformation, Genetic


  • Antibodies, Monoclonal
  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Surface
  • Histocompatibility Antigens Class II
  • Macromolecular Substances
  • Peptides
  • Polymers
  • GAT