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Authors
Guðmundur Jóhann ArasonIssue Date
2008-05-01
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The association of complement with common connective tissue diseases - a reviewCitation
Læknablaðið 2008, 94(5):371-4Abstract
A strong association has been found between complement and common connective tissue diseases, such as systemic lupus erythema and Henoch Schoenlein Purpura. This has led to the notion that the pathogenesis of such diseases may involve a defect in the safe disposal of immune complexes, which is mediated by complement. To bring further light on this subject, a sensitive assay was developed to measure the ability of serum to prevent immune precipitation. This assay was then employed to study various Icelandic patient groups, and a defect in this function of complement was found to be common in patients with systemic lupus erythematosus and systemic sclerosis. Partial deficiency in complement C4A (C4A Q0) can not account for this defect, as it was not observed in patients with diabetes, gluten-sensitive enteropathy or autoimmune thyroiditis, in which C4A Q0 is common. The defect is strongly correlated with anti-C1q antibodies. Further studies are needed to test the possible role of anti-C1q antibodies in the pathogenesis of immune complex disease.Sterk tengsl hafa greinst milli magnakerfis og algengra bandvefssjúkdóma, svo sem rauðra úlfa og Henoch Schönlein Purpura. Þetta hefur leitt til hugmynda um að galli í virkni magnakerfis geti átt þátt í meinferli slíkra sjúkdóma, og er þá einkum litið til hlutverks kerfisins í eyðingu mótefnafléttna. Til að varpa ljósi á málið var þróað próf sem mælir getu blóðvökva til að halda mótefnafléttum í lausn. Þessu prófi hefur verið beitt á ýmsa hópa íslenskra sjúklinga og reyndist gölluð meðhöndlun mótefnafléttna algeng í rauðum úlfum og herslismeini. Vantjáð afurð C4A-gens (C4A*Q0) nægir ekki til að skýra þennan galla því hann finnst ekki í sjúklingum með sykursýki, glútenóþol eða skjaldkirtilssjúkdóm, þrátt fyrir háa tíðni C4A*Q0 í þessum hópum. Gallinn hefur á hinn bóginn sterka fylgni við hækkuð mótefni gegn C1q. Frekari rannsókna er þörf til að skera úr um hvort mótefni gegn C1q geti átt þátt í meinþróun sjúkdómsins
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