NURS 6501: MIDTERM EXAM:
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The mucosal damage observed in celiac disease is primarily the result of:
Group of answer choices
- Cell-mediated immune response to deamidated gliadin peptides
- Complement system activation secondary to gluten deposition
- Direct toxicity of gluten peptides to enterocytes
- IgE-mediated allergic reaction to gluten
- Gliadin peptides (a protein fraction of gluten) are ingested and undergo deamidation by the enzyme tissue transglutaminase (tTG) in the small intestine.
- The deamidated gliadin peptides are recognized by HLA-DQ2 or HLA-DQ8 on antigen-presenting cells.
- This recognition triggers a T-cell-mediated immune response, resulting in the release of inflammatory cytokines.
- The immune response leads to villous atrophy, crypt hyperplasia, and inflammation of the small intestine mucosa, causing the classic symptoms of celiac disease, such as chronic diarrhea, malabsorption, and nutrient deficiencies.
- Complement system activation secondary to gluten deposition: While the immune response in celiac disease involves inflammation, complement activation is not the primary mechanism. The primary issue is T-cell-mediated inflammation rather than complement activation.
- Direct toxicity of gluten peptides to enterocytes: Gluten itself is not directly toxic to enterocytes. The damage is mediated by the immune system targeting the deamidated gliadin peptides and the subsequent inflammatory response.
- IgE-mediated allergic reaction to gluten: Celiac disease is not an IgE-mediated allergic reaction. It is a T-cell-mediated autoimmune disorder. IgE-mediated reactions typically occur in food allergies, but celiac disease involves autoimmunity rather than an allergic response.
