Expression of Cell-Adhesion Molecules in the Salivary Gland Microenvironment of Sjögren's Syndrome

Authors

  • E. William S.T. Clair MD,

    Corresponding author
    1. Division of Rheumatology and Immunology, Department of Medicine, the Division of Plastic, Reconstructive, Maxillofacial, and Oral Surgery, Department of Surgery, and the Department of Microbiology and Immunology, Duke University Medical Center, Durham, North Carolina.
    • Box 3874, Duke University Medical Center, Durham, NC 27710
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  • John C. Angellilo MD, DDS,

    1. Division of Rheumatology and Immunology, Department of Medicine, the Division of Plastic, Reconstructive, Maxillofacial, and Oral Surgery, Department of Surgery, and the Department of Microbiology and Immunology, Duke University Medical Center, Durham, North Carolina.
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  • Kay H. Singer PhD

    1. Division of Rheumatology and Immunology, Department of Medicine, the Division of Plastic, Reconstructive, Maxillofacial, and Oral Surgery, Department of Surgery, and the Department of Microbiology and Immunology, Duke University Medical Center, Durham, North Carolina.
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Abstract

Objective. The potential role of cell adhesion molecules in the pathogenesis of Sjögren's syndrome (SS) was assessed by examining their expression in salivary gland (SGL) tissue.

Methods. Intercellular adhesion molecule type 1 (ICAM-1), lymphocyte function-associated antigen type 1 (LFA-1), LFA-3, CD2, and CD44 expression were determined using indirect immunofluorescence techniques.

Results. In inflamed labial SGL tissue, ICAM-1 expression was evident on infiltrating LFA-1+/CD2+/LFA-3+ mononuclear cells, and to a limited extent on SGL acinar epithelial cells adjacent to sites of intense inflammation.

Conclusion. In SS, the SGL microenvironment is characterized by only a modest up-regulation of ICAM-1 expression on epithelial cells, despite the presence of T cells bearing an activated phenotype.

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