C1q and
mannose binding lectin, members of the "defense
collagen" family, are pattern recognition molecules that can trigger rapid enhanced phagocytosis resulting in efficient containment of pathogens or clearance of cellular debris, apoptotic cells and
immune complexes. In addition, interaction of C1q and
mannose binding lectin with the phagocyte alters subsequent phagocyte
cytokine synthesis, and thus may have important implications in directing acute
inflammation as well as long-term protective immunity. The importance of the role of defense
collagens in phagocytosis of apoptotic cells is highlighted by studies in vivo of mice deficient in C1q,
pulmonary surfactant D and
mannose binding lectin in which there is delayed clearance of apoptotic cells. Indeed, deficiency of C1q is a risk factor for the development of autoimmunity in both humans and mice, consistent with the hypothesis that inefficient clearance of apoptotic cells results in release of
autoantigens and contributes to the pathology associated with
autoimmune diseases such as
systemic lupus erythematosus. Further understanding of the importance of C1q and
mannose binding lectin in the clearance of apoptotic cells and regulation of
cytokine synthesis and identification of the receptors implicated in mediating these processes should provide novel targets for therapeutic intervention in the control and manipulation of the immune response in terms of both host defense against
infectious disease and tissue repair and remodeling.