While Relatively Rare, Individuals with a Homozygous Deficiency in Complement

Multiple Choice

While relatively rare, individuals with a homozygous deficiency in complement C1 activity have been identified, and >90% of them developed a lupus-like illness at a very young age. These individuals had significant kidney damage and damage to blood vessels in the central nervous system, both of which were associated with severe inflammation. A reasonable hypothesis to explain the development of the lupus-like disease in these patients is:

A) Immune complex-mediated activation of the classical complement pathway
B) Trapping of immune complexes in small blood vessels that block blood flow, leading to necrosis
C) A non-immune function of C1 that is unrelated to the complement pathway
D) A failure of immune complexes lacking complement deposition on them to bind to phagocyte Fc receptors
E) A role for the complement pathway in clearing apoptotic cells from the circulation