Properdin (complement factor P) is a conserved serum glycoprotein of the immune defence. It plays a role in strengthening the activation of complement, a system of proteins important in the first line defence against infection. Properdin is active in the alternative pathway of complement within the innate immune system. It is the sole regulator of complement activation and plays a major role in regulating the alternative pathway by binding to and stabilising the inherently labile C3 convertase enzymes, C3bBb and C3bBbC3b. The properdin-deficient mouse line was used in various studies in order to investigate the role of properdin in disease models of immunity, infection and inflammation. It was shown that properdin controls the strength of immune responses by affecting both humoral and cellular phenotypes during acute bacterial infection and resulting inflammation. A clear overview of the measurements for which properdin-deficient and wild-type mice are similar or different in their unstimulated state is lacking. This review shows the cumulative analysis in mouse regarding the effect of properdin-deficiency on baseline immune measurements, and will consider all studies on properdin-deficient and wild-type mice, where inflammatory cellular or humoral mediators, activities and metabolism were measured. The analysis lends support to the concept that systemic therapeutic targeting of properdin may influence properdin-dependent cellular crosstalks within tissues.
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