Up-regulation of alphaEbeta7, a novel integrin adhesion molecule, on T cells from systemic lupus erythematosus patients with specific epithelial involvement

Arthritis Rheum. 1998 Aug;41(8):1456-63. doi: 10.1002/1529-0131(199808)41:8<1456::AID-ART16>3.0.CO;2-0.

Abstract

Objective: To determine the possible role of a novel integrin, alphaEbeta7, in the pathogenesis of systemic lupus erythematosus (SLE).

Methods: Expression of alphaEbeta7 was examined on peripheral blood lymphocytes (PBL) from normal subjects (n = 25) and patients with SLE (n = 31), primary Sjogren's syndrome (n = 7), or polymyositis/dermatomyositis (n = 8) by cytofluorometry and/or immunoprecipitation. Adhesion of alphaEbeta7+ T cells to HSG epithelial cells was investigated using a confocal image analyzer.

Results: After phytohemagglutinin stimulation, expression of alphaEbeta7 on PBL, especially on CD8+ T cells, was significantly higher in SLE patients than in normal subjects (P<0.01). Elevated alphaEbeta7 expression was associated with the presence of oral ulcers or serositis (P<0.05). Activated SLE T cells with enhanced alphaEbeta7 expression strongly adhered to HSG; this adhesion was partially blocked by anti-alphaEbeta7.

Conclusion: Expression and adhesion of alphaEbeta7 on activated PBL was significantly increased in patients with SLE with epithelial involvement. This suggests a role of this novel integrin in tissue-specific retention of activated PBL, due to increased alphaEbeta7-E-cadherin interaction, which may contribute to epithelial inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antigens, CD / metabolism*
  • Autoimmune Diseases / metabolism
  • Cell Adhesion / physiology
  • Cell Line
  • Epithelial Cells / physiology
  • Epithelium / pathology
  • Female
  • Humans
  • Integrin alpha Chains*
  • Lupus Erythematosus, Systemic / complications
  • Lupus Erythematosus, Systemic / metabolism*
  • Lupus Erythematosus, Systemic / pathology
  • Male
  • Oral Ulcer / etiology
  • Serositis / etiology
  • T-Lymphocytes / metabolism*

Substances

  • Antigens, CD
  • Integrin alpha Chains
  • alpha E integrins