What would a patient deficient in the C3 complement component be expected to mount a normal response to?

A patient deficient in the C3 complement component would likely mount a normal response to type I and type IV hypersensitivity reactions. This is because types I and IV hypersensitivity responses are mediated primarily by mechanisms that do not heavily rely on the complement system.

Type I hypersensitivity involves IgE antibodies, which lead to allergic responses mediated by mast cells and basophils rather than complement activation. In these reactions, the presence of IgE triggers the release of histamines and other mediators from mast cells, independent of C3.

Type IV hypersensitivity is mediated by T cells and does not involve antibodies or the complement system. It is a delayed-type hypersensitivity reaction resulting from T-cell activation and the subsequent recruitment of macrophages, which does not rely on the components of the complement pathway, including C3.

In contrast, a deficiency in C3 would significantly impact the body’s ability to clear immune complexes and activate effector functions associated with type II (cytotoxic antibody-mediated) and type III (immune complex-mediated) hypersensitivity reactions, where complement plays a critical role in opsonization, inflammation, and clearance of pathogens and immune complexes. Thus, the immune mechanisms involved in these types of hypersensitivity rely more on the complement pathway, meaning that