Sjögren's syndrome. Autoimmune epithelitis

Area of Science:

• Immunology
• Pathology
• Autoimmune Diseases

Background:

• Sjögren's syndrome is a chronic autoimmune disorder affecting exocrine glands.
• Characterized by mononuclear cell infiltration of epithelial cells.
• Understanding the immunopathologic lesion is crucial for Sjögren's syndrome research.

Purpose of the Study:

• To investigate the role of epithelial cells and infiltrating immune cells in Sjögren's syndrome pathophysiology.
• To analyze the expression of specific molecules involved in inflammation, apoptosis, and regeneration.

Main Methods:

• Analysis of mononuclear cell populations (CD4+ T lymphocytes, B cells) in salivary gland lesions.
• Assessment of epithelial cell expression of cytokines (IL-1β, IL-6), protooncogenes (c-myc), and costimulatory molecules (B7-1, B7-2).
• Evaluation of apoptosis-related molecules (Fas, FasL, Bax, Bcl-2, Perforin, Granzymes) and trefoil proteins (pS2) in epithelial and mononuclear cells.

Main Results:

• Mononuclear cells, primarily CD4+ T lymphocytes (60-70%) and B cells (25%), infiltrate salivary glands.
• Epithelial cells express pro-inflammatory cytokines, protooncogenes, and costimulatory molecules.
• Evidence suggests epithelial cell apoptosis via Fas/FasL and Bax pathways, counteracted by mononuclear cell Bcl-2, Perforin, and Granzymes.
• Epithelial cells also express trefoil proteins (pS2), indicating a regenerative effort.

Conclusions:

• Epithelial cells are significantly involved in Sjögren's syndrome pathophysiology, exhibiting both susceptibility to damage and regenerative capacity.
• The interplay between epithelial cell apoptosis and immune cell infiltration is central to the disease.
• The precise triggers for the autoimmune response in Sjögren's syndrome remain to be elucidated.