Absence of an association between mannose-binding lectin polymorphism and rheumatoid arthritis |
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Authors: | Stanworth SJ; Donn RP; Hassall A; Dawes P; Ollier W; Snowden N |
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Institution: | Department of Clinical Immunology, St Mary's Hospital, Manchester. |
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Abstract: | It has been proposed that mannose-binding lectin (MBL) interactions with
agalactosyl forms of IgG immunoglobulins found in rheumatoid synovial fluid
might lead to enhanced complement activation, an important mediator of the
joint damage in rheumatoid arthritis (RA). In order to investigate this
possible link between increased MBL-mediated activation of complement and
perpetuation of rheumatoid synovitis, we have compared the frequency of an
allelic form of MBL, known to be incapable of activating complement, in a
group of hospital patients with severe RA and control subjects. No evidence
was found to support an association between the presence of this MBL allele
and protection from rheumatoid disease; genotype frequencies were similar
in both groups. This suggests that complement activation via
MBL-agalactosyl IgG complexes is unlikely to play a major role in the
pathophysiology of RA.
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