The membrane complement regulatory protein CD59 and its association with rheumatoid arthritis and systemic lupus erythematosus

The complement cascade consisting of about 50 soluble and cell surface proteins is activated in autoimmune inflammatory disorders. This contributes to the pathological manifestations in these diseases. In normal health, the soluble and membrane complement regulatory proteins protect the host against complement-mediated self-tissue injury by controlling the extent of complement activation within the desired limits for the host's benefit. CD59 is a membrane complement regulatory protein that inhibits the formation of the terminal complement complex or membrane attack complex (C5b6789n) which is generated on complement activation by any of the three pathways, namely, the classical, alternative, and the mannose-binding lectin pathway. Animal experiments and human studies have suggested importance of membrane complement proteins including CD59 in the pathophysiology of rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Here is a brief review on CD59 and its distribution, structure, functions, and association with RA and SLE starting with a brief introduction on the complement system, its activation, the biological functions, and relations of membrane complement regulatory proteins, especially CD59, with RA and SLE.