The complement system is a crucial part of the innate immune system, it recognizes many non-self structures present on pathogens or altered self cells. The initiation of the complement system elicits proteolytic cascades which finally leads to the cleavage of the C5 protein into two fragments, C5a and C5b. C5a is a small anaphylatoxin that can cause a variety of biological responses upon binding to the 7TM receptors C5aR and the C5L2. However, C5b is a big fragment nucleates generation of the membrane attack complex which enables to kill susceptible pathogens via the production of a pore structure in association with complement components C6, C7, C8, and C9.
Fig. 1 Activation of C5 by C5 convertase leads to the generation of C5a and C5b.1, 2
Generally, a range of regulatory molecules help to regulate C5 mediated immune responses towards host cells. However, in many major inflammatory conditions (e.g., sepsis and arthritis), C5a is demonstrated to contribute significantly to disease etiology. In the past years, several attempts have been made to develop inhibitors of complement C5 activation. These inhibitors target factors upstream of C5, such as complement components C5, C5 convertase, C5a, and C5b, as well as C5a receptor. Nowadays, a full range of types of antibodies and compounds have actively been developed. These inhibitors may be effective at treating various inflammatory diseases involving complements.
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