The complement system is a key part of our immune system, helping to fight infections and protect the body. It reacts quickly to germs, even before our main immune response kicks in. This system is made up of many proteins and receptors, such as C3, C3b, and iC3b, which are found in the blood, tissues, and different body fluids.
Exploring the Three Pathways of Complement Activation
The complement system can be activated in three different ways. First, the classical pathway starts when immune complexes are present. Second, the lectin pathway begins with lectins attached to surfaces. Third, the alternative pathway (AP) is triggered on unprotected surfaces. All these pathways create a special enzyme called C3 convertase. This enzyme is important because it cuts the main protein, C3, into a smaller piece known as C3b.
The C3 and C5 convertases are enzymatic complexes that initiate and amplify the activity of the complement pathways, leading to the generation of the cytolytic membrane attack complex (MAC). The synthesis of C3, including its forms C3b and iC3b, is tissue-specific and modulated in response to various stimulatory agents. Upon cleavage by C3 convertase, the anaphylotoxin C3a and the activating fragment C3b are formed. C3b, when bound to the cell surface, initiates the terminal pathway of complement by forming the C5 convertase.
Understanding C3, C3b, and iC3b: Crucial Components of Immune Defense
C3, with a molecular weight of approximately 185kDa, is the most abundant protein in the complement system, featuring serum protein levels of about 1.3 mg/ml. Primarily produced by the liver, C3, as well as its derivatives C3b and iC3b, are also synthesized in macrophages, neutrophils, endothelial, and epithelial cells. Due to its high levels in circulation and low biological reactivity, C3/C3b/iC3b acts swiftly and potently in response to dangers, such as pathogen encounters.
However, defects in C3/C3b/iC3b can be detrimental, leading to recurrent infections or autoimmune diseases. C3 deficiency is uncommon, but it does happen. This deficiency affects how well C3b and iC3b work. It leads to frequent infections and problems with the development of immune cells. Polymorphisms in C3 have been associated with conditions like age-related macular degeneration (AMD) and atypical hemolytic uremic syndrome (aHUS). Beyond pathogen clearance, C3/C3b/iC3b plays a vital role in the removal of circulating immune complexes, aiding the phagocytic capacity of macrophages. Malfunctions in this system can lead to autoimmune diseases and complement deposition in tissues.
Not sure which C3 antibody to use?
With numerous options available, it is essential to select the right C3 antibody to ensure the success of your research. We designed a guide to assist you in making an informed decision:
Go to our C3 researcher’s guide and choose the right antibody
Immuno assays, Western blot
- IA: Antibody 18.1 can be used as detection antibody.
- W: Reduced and Non-reduced western blot can be performed. Pending the quality of samples, be aware that several breakdown products can be visible.
Dilutions to be used depend on detection system applied. It is recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:50.