NURS 6501: MIDTERM EXAM: Please contact Your Favorite Professor for help with   NURS 6501: Midterm Exam or any other assignment. Email: professorrobertphd@gmail.com   A 28-year-old female presents with chronic diarrhea, steatorrhea, and anemia. She is diagnosed with celiac disease. Which of the following is the primary immunological mechanism leading to villous atrophy in celiac disease? Group of answer choices

• IgE-mediated allergic reaction to gluten
• Complement activation due to IgM deposits in the duodenum
• T-cell-mediated immune response to gluten
• Autoantibody production against parietal cells

  The correct answer is T-cell-mediated immune response to gluten. Explanation: Celiac disease is primarily characterized by an immune-mediated reaction to gluten, a protein found in wheat, barley, and rye. The disease involves a T-cell-mediated immune response, particularly CD4+ T cells, which are activated by the presentation of gluten peptides by HLA-DQ2 or HLA-DQ8 molecules on the surface of antigen-presenting cells in the small intestine. The process leads to:

1. Activation of T cells: Gluten-derived peptides are deamidated by tissue transglutaminase (tTG) and presented by HLA molecules to T cells in the lamina propria of the small intestine.
2. Inflammation and damage: Activated T cells release cytokines that lead to inflammation and ultimately cause villous atrophy and crypt hyperplasia in the small intestine, impairing nutrient absorption and leading to symptoms like chronic diarrhea, steatorrhea (fatty stools), and anemia.

Why the other options are incorrect:

• IgE-mediated allergic reaction to gluten: This describes a type I hypersensitivity reaction (common in conditions like food allergies), but celiac disease involves T-cell-mediated immunity, not IgE. Celiac disease is not an IgE-mediated allergic reaction.
• Complement activation due to IgM deposits in the duodenum: This is not a feature of celiac disease. Celiac disease primarily involves T-cell activation and does not involve complement activation through IgM deposits.
• Autoantibody production against parietal cells: This occurs in autoimmune gastritis, not celiac disease. In celiac disease, autoantibodies are produced against tissue transglutaminase (tTG), not parietal cells.

Thus, the primary immunological mechanism leading to villous atrophy in celiac disease is the T-cell-mediated immune response to gluten.