C3, 3rd Component of Complement, Serum/Plasma

C3 is the central component of the complement system, which comprises around 20 soluble components, which is active in both the acquired and innate immune systems. In acquired immunity, the complement system is activated by antibodies bound to foreign material (classical pathway). In innate immunity, the system can be activated, in a similar manner, by the mannan binding lectin (MBL), which recognises foreign carbohydrate structures (MBL pathway), and also by a mechanism that involves the differential interaction with self and non-self surface structures (alternative pathway). The functions of complement in innate immunity range from chemoattraction of leukocytes to the site of infection and the enhancement of phagocyte effector activities to direct destruction of certain microorganisms. The covalent binding of C3 to activating surfaces is responsible for initiating most of the effects of the system.

The following are disorders associated with complement activation: systemic inflammatory reaction syndrome, multiple organ dysfunction syndrome, ischemia reperfusion syndrome, angioedema, capillary leak syndrome, hyperacute and acute graft rejection, vasculitis, nephritis, autoimmune disorders (e.g., SLE, rheumatoid arthritis, and myasthenia gravis), biomaterial incompatibility (e.g., following dialysis or cardiopulmonary bypass), and severe trauma, burn, and sepsis. Recently, complement has been implicated in neurodegenerative disorders, such as Alzheimer’s disease, multiple sclerosis, and Guillain-Barre syndrome. Complement defects may be the cause of immunodeficiency mediated recurrent infections.

1 ml Serum 1 ml Li, NH4+-Heparin Plasma Stability: 4 Days at 15-25 °C 8 Days at 2-8 °C 8 Days at (-15)-(-25) °C

Separate serum/plasma from cells as soon as possible.

90 - 180 mg/dL 0.9 - 1.8 g/L