C1q, a subcomponent of the classical complement pathway, mediates its activation and thereby plays an important role in immune response. The presence of receptors for C1q on effector cells modulates its activity, which may be antibody-dependent or independent. Macrophages are the primary source of C1q, and anti-inflammatory drugs as well as cytokines differentially regulate expression of the mRNA as well as the protein. However, its ability to modulate the interaction of platelets with collagen and immune complexes suggests C1q influences homeostasis as well as other immune activities, and perhaps thrombotic complications resulting from immune injury.