Lack of proliferative response by gluten-specific T cells in the blood and gut of patients with dermatitis herpetiformis

J Autoimmun. 1995 Aug;8(4):561-74. doi: 10.1016/0896-8411(95)90008-x.

Abstract

The majority of patients with Dermatitis Herpetiformis (DH) have a gluten-sensitive enteropathy which may be triggered by a T cell-mediated immune response to gluten. Using a proliferative assay, the responses to gluten fraction III, recall antigens and mitogens of peripheral blood mononuclear cells (PBMC) and gut T cell lines (TCL) isolated from patients with Dermatitis Herpetiformis (DH) and normal controls were studied. In most cases, neither PBMC nor gut T cell lines (which were predominantly CD3+, CD4+, TCR alpha beta +) from either controls or patients proliferated in response to gluten fraction III alone. However, the addition of 10 U/ml IL-2 to PBMC cultures containing gluten fraction III resulted in a marked increase in proliferation in 9/19 DH patients and 7/11 controls compared to IL-2 alone. Furthermore, gluten-induced upregulation of IL-2 receptor (CD25) expression was demonstrated on PBMC from 4/4 patients with DH and 2/3 controls after 7 days' culture with antigen. A similar effect by exogenous IL-2, or the same concentration of IL-4, was observed in 8/11 (P = 0.02) and 5/6 respectively DH, and 3/4 normal gut T cell lines. No difference was observed in the response of DH and control PBMC to Tetanus toxin, Candida albicans and PPD; both normal and DH gut T cell lines were unresponsive to these antigens. However, the addition of IL-2 increased the response to Candida albicans by DH gut T cell lines. Moreover, the response of DH gut T cell lines to PHA (P < 0.001), Concanavalin A and anti-CD3 were markedly reduced compared to PBMC from the same patients. These findings suggest that gluten-specific T cells present in the blood and gut of normal and DH individuals are activated by but do not proliferate in response to specific antigen.

MeSH terms

  • Candida albicans / immunology
  • Cell Line
  • Dermatitis Herpetiformis / blood
  • Dermatitis Herpetiformis / immunology*
  • Fluorescent Antibody Technique, Indirect
  • Glutens / immunology*
  • Glutens / pharmacology
  • Humans
  • Immunologic Memory
  • Interleukin-2 / pharmacology
  • Interleukin-4 / pharmacology
  • Intestine, Small / immunology
  • Leukocytes, Mononuclear / immunology
  • Lymphocyte Activation* / drug effects
  • Mitogens / pharmacology
  • Receptors, Interleukin-2 / metabolism
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / immunology*
  • Tetanus Toxoid / pharmacology
  • Tuberculin / pharmacology

Substances

  • Interleukin-2
  • Mitogens
  • Receptors, Interleukin-2
  • Tetanus Toxoid
  • Tuberculin
  • Interleukin-4
  • Glutens