Abstract
Background: Complement proteins constitute a proinflammatory system of the innate immunity which bridges with the adaptive immunity. It comprises of a group of serum zymogens, complement regulatory proteins (Cregs) and receptors. Most of the Cregs, namely CD59, CR1, DAF and MCP are membrane bound. Their soluble forms circulate in the body fluids. Activation of the zymogens through three distinct but interconnected pathways generate functionally important peptides. Most of the effects are produced by the interaction of the active peptides with their cell surface receptors. Uncontrolled activation of the system due to the overburdening triggers and deficient regulatory mechanisms leads to self-tissue injury in autoimmune and inflammatory disorders. Modulation of the Cregs has been evidenced in systemic rheumatoid disorders.
Objective: This review is an attempt to collate the literature culminated and insight gained regarding the association of CD59, a membrane Creg with the pathophysiology of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) and its potential as a biomarker and therapeutic target for these two diseases.
Methodology: This review enfolds the information obtained from the original primary research papers, citations and review articles including our own laboratory findings and publications with key search from the PUBMED. Although CD59 has been implicated in several diseases, here our search remained focused only to SLE and RA.
Results: Evidences suggest disease related modulation and protective role of CD59 in SLE and RA. The bulk of information came from the animal studies.
Conclusions: An intimate relation of CD59 with the pathophysiology of SLE and RA is envisaged. CD59 appears to hold promise as a biomarker and therapeutic target for these two autoimmune disorders. More studies on human subjects along with supportive evidences from the animal models are needed. Modulation of CD59 expression by cytokines opens up a new avenue in the context.
Keywords
CD59, Complement, Creg, SLE, RA, Pathophysiology