A 32-year-old woman with a 3-year history of systemic lupus erythematosus presents to the emergency department with acute onset dyspnea, pleuritic chest pain, and low-grade fever. She reports recent medication non-adherence. Vital signs: BP 128/82 mmHg, HR 102/min, RR 22/min, temperature 37.8°C, SpO2 98% on room air. Chest X-ray shows bilateral pleural effusions. Pleural fluid analysis demonstrates: LDH 320 U/L (serum LDH 240 U/L), protein 3.2 g/dL, glucose 68 mg/dL, positive ANA, positive anti-dsDNA antibodies, and decreased complement C3 (42 mg/dL; normal 80-160). Serum creatinine is 0.9 mg/dL and urinalysis shows no proteinuria. Which of the following best explains the pathophysiology of pleural inflammation in this patient?

1. A)Deposited immune complexes activate the complement cascade, generating C5a chemotaxins that recruit neutrophils, which release proteolytic enzymes causing tissue damageGABARITO
2. B)Autoreactive T cells directly infiltrate the pleura and release interferon-gamma, causing delayed hypersensitivity tissue damage
3. C)Anti-pleural mesothelial cell antibodies directly bind mesothelial cells and activate complement-dependent cellular cytotoxicity
4. D)Circulating anti-dsDNA antibodies cross-react with pleural surface antigens, initiating mast cell degranulation and local histamine release
5. E)Neutrophil elastase released from activated neutrophils causes direct proteolytic damage independent of immune complex deposition