IMMUNE DYSREGULATION AND EPITHELIAL STRESS IN CELIAC DISEASE PROGRESSION: A FOCUS ON REFRACTORY CELIAC DISEASE...

Area of Science:

• Gastroenterology
• Immunology
• Cell Biology

Background:

• Celiac disease (CD) is an autoimmune disorder triggered by gluten, causing small intestine damage.
• Refractory celiac disease (RCD) is a non-responsive form of CD with unclear mechanisms.
• Distinguishing RCD from CD is crucial for effective patient management.

Purpose of the Study:

• To investigate immunohistochemical differences between CD and RCD.
• To identify markers of immune dysregulation and epithelial stress in RCD.
• To explore potential biomarkers for RCD severity and progression.

Main Methods:

• Retrospective analysis of 93 patients with CD (Marsh stages 1-3b) and RCD (Type I and II).
• Immunohistochemical examination of tissue samples for CD3, CD8, CD103, FOXP3, Ki-67, MHC I, and MHC II.
• Comparative analysis of marker expression across different disease stages and subtypes.

Main Results:

• Progressive immune activation and epithelial stress correlate with increased disease severity.
• A significant decrease in FOXP3-positive regulatory T cells was observed in RCD, particularly Type II.
• Elevated Ki67 indices and upregulated MHC II expression were noted in advanced CD and RCD stages.

Conclusions:

• Immune dysregulation and epithelial stress are key factors in CD to RCD transition.
• Decreased FOXP3+ T cells, increased Ki67, and heightened MHC II expression may serve as biomarkers for RCD.
• Targeting these pathways offers potential for improved RCD management strategies.