Inflammation and Immune Pathology USMLE Step 1 Practice Question
A 52-year-old man with a 30-year occupational history of asbestos exposure presents to the pulmonary clinic with progressive dyspnea, chest pain, and persistent dry cough. Vital signs are notable for RR 22 and SpO2 88% on room air. High-resolution CT chest demonstrates bilateral lower lobe interstitial fibrosis with pleural thickening and calcified pleural plaques. Pulmonary function testing shows a restrictive pattern with reduced FVC and FEV1/FVC ratio > 0.75. Lung biopsy reveals extensive collagen deposition, myofibroblast activation, and numerous foamy macrophages within alveolar spaces and fibrotic tissue. Which of the following cell types and mediators most directly explains the progressive fibrotic pathology in this patient's asbestos-induced pulmonary disease?
Answer choices
- AAlveolar macrophages activated by asbestos fibers, secreting transforming growth factor-beta and tumor necrosis factor-alphaCorrect answer
- BTissue mast cells degranulating in response to asbestos, releasing histamine and tryptase
- CB lymphocytes producing asbestos-specific IgE and IgG antibodies against fiber antigens
- DNeutrophils recruited to the lung parenchyma, generating reactive oxygen species and proteases
- ECD8+ cytotoxic T lymphocytes recognizing asbestos-coated epithelial cells and inducing apoptosis
- FEosinophils infiltrating the airways, releasing major basic protein and eosinophil peroxidase
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