A 35-year-old woman presents to the clinic with a 6-month history of progressive fatigue, symmetric joint pain in her hands and knees. She reports that she develops malar rash that worsens with sun exposure. She also reports occasional fevers and hair loss. She denies any history of renal dysfunction or neurologic symptoms. Her vitals are heart rate 87 beats/minute and blood pressure 125/78 mmHg. Laboratory tests reveal positive antinuclear antibodies at a titer of 1:640, positive anti-double-stranded deoxyribonucleic acid antibodies, low complement C3 and C4 levels, and an elevated erythrocyte sedimentation rate. A skin biopsy from the affected area shows immune complex deposition at the dermo-epidermal junction.
Which of the following is the most likely mechanism of tissue damage in this condition?
D) Type III hypersensitivity
The clinical presentation, including malar rash, joint pain, and positive autoantibodies, along with low complement levels and immune complex deposition on biopsy, is consistent with systemic lupus erythematosus (SLE). Type III hypersensitivity involves the formation of antigen-antibody immune complexes that deposit in tissues, such as the skin, joints, and kidneys, triggering complement activation and inflammation, which is the primary mechanism of tissue damage in systemic lupus erythematosus.
Answer choice A: Direct cytotoxic T-cell-mediated damage is incorrect. Direct cytotoxic T-cell-mediated damage, seen in conditions like viral infections or graft rejection, involves T cells directly targeting infected or foreign cells, not immune complex deposition or complement activation as seen in this case.
Answer choice B: Type I hypersensitivity is incorrect. Type I hypersensitivity is immunoglobulin E-mediated, leading to immediate allergic reactions such as anaphylaxis or asthma.
Answer choice C: Type II hypersensitivity is incorrect. Type II hypersensitivity involves antibodies targeting cell surface or extracellular matrix antigens, as in autoimmune hemolytic anemia or myasthenia gravis.
Answer choice E: Type IV hypersensitivity is incorrect. Type IV hypersensitivity is T-cell-mediated and delayed, as in contact dermatitis or tuberculosis, and does not involve immune complexes or complement activation.
Key Learning Point
Systemic lupus erythematosus involves type III hypersensitivity, where immune complexes deposit in tissues, triggering complement activation and inflammation, leading to symptoms like malar rash, arthritis, and low complement levels.
