Beta-cell antigen-specific lysis of macrophages by CD4 T-cell clones from newly diagnosed IDDM patient. A putative mechanism of T-cell-mediated autoimmune islet cell destruction

Diabetes. 1992 Nov;41(11):1380-4. doi: 10.2337/diab.41.11.1380.

Abstract

Immunophenotyping of the early lesion in the pancreatic islets of Langerhans demonstrates a predominance of CD4+ lymphocytes, which may be preceded by an increase in islet macrophages. This observation implies that both types of cells may be involved in autoimmune-mediated beta-cell destruction leading to IDDM. In an attempt to attribute a role to beta-cell antigen-specific CD4-expressing T-cell clones recently isolated from a newly diagnosed IDDM patient, we investigated whether such CD4 T-cells may be pathogenic in an in vitro cytotoxicity assay with HLA-DR-matched antigen-presenting macrophages as target. We report herein that, indeed, beta-cell antigen-specific CD4+ T-cells are capable of lysing macrophages in an antigen-specific fashion. This cytotoxicity is HLA-DR restricted, T-cell receptor complex mediated, and CD4 dependent. These observations imply that both helper T-cells and macrophages may be involved in the disease process via interaction between T-cells and macrophages pulsed with beta-cell antigen.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoimmunity*
  • CD4 Antigens / immunology*
  • Cell Membrane / immunology
  • Cells, Cultured
  • Clone Cells
  • Cytotoxicity, Immunologic*
  • Diabetes Mellitus, Type 1 / blood
  • Diabetes Mellitus, Type 1 / immunology*
  • HLA-DR Antigens / immunology
  • Humans
  • Insulinoma / immunology
  • Islets of Langerhans / immunology*
  • Macrophages / immunology*
  • Pancreatic Neoplasms / immunology
  • Rats
  • T-Lymphocyte Subsets / immunology*

Substances

  • CD4 Antigens
  • HLA-DR Antigens