Answer: a, c, d Complement activation can occur through either classic or alternate (properdin) pathways, both of which eventuate in deposition of terminal complement pathway components on the antigenic cell surface. The classic pathway of complement activation usually begins with immunoglobulin G-binding which has also bound the antigen. The alternate pathway activation occurs in response to activation of direct binding of the antigen or directly through contact with fungal and bacterial cell wall compounds such as zymosan and gram-negative bacterial lipopolysaccharide (LPS endotoxin). Several complement components represent important host defenses acting to recruit or augment cellular host defenses or to directly inactivate invading microbes through lytic activity. The production of complement component fractions C3a and C5a during activation of this cascade serve primarily to markedly increase vascular permeability, and C5a functions as a PMN and macrophage chemoattractant. This process leads to the recruitment of additional humoral and cellular defenses to the specific area of infection. Excessive complement activation can produce deleterious effects in some instances. Complement activation causes enhanced PMN adhesion, margination, and release of lysosomal enzymes that can directly damage certain target tissues, such as the lung