The complement system in rheumatoid synovitis i. an analysis of complement component activities in rheumatoid synovial fluids

Abstract

Stoichiometric hemolytic assays were used to measure the activities of the first four reacting cmponents of the complement sequence in synovial fluids from patients with seropositive or seronegative rheumatoid arthritis or degenerative joint disease. The pattern of component reductions in the seropositive rheumatoid arthritis fluids was consistent with activation of the complement system by an intra-articular immunologic process.

Clinical correlations with serum C1q levels in patients with rheumatoid arthritis

“…However, in the present study, Clq levels were significantly lower in synovial fluid than in paired plasma samples, which is consistent with previously reported data indicating that very low levels of C 1 q are present in some RA synovial fluids as a result of avid binding of free Clq by immune complexes (17). Furthermore, precipitin lines can be developed between RA serum and RA synovial fluid, consistent with the presence of free Clq in the blood and of complexes that bind Clq in the synovial fluid (18).…”

Mast cells contribute to initiation of autoantibody-mediated arthritis via IL-1

“…In seropositive RA, unlike in other inflammatory arthritides, such as gout or psoriatic arthritis, deposition of immune complexes is typically observed in synovium and cartilage, whereas joint effusions exhibit prominent consumption of complement (5,36,37). Similarly, circulating and synovial fluid immune complexes may be demonstrated in the majority of patients (5,38).…”

Circulating complement breakdown products in patients with rheumatoid arthritis. Correlation between plasma C3d, circulating immune complexes, and clinical activity.

“…Evidence of the involvement of these two factors in RA is mainly derived from studies of the joint spaces with demonstration of depressed synovial fluid complement levels and presence of immune complexes in the synovium and in synovial fluid (1)(2)(3)(4) (4)(5)(6). However, the level of complement components is generally normal or increased in plasma from BA patients (1,7,8). This finding has been explained by an increased synthesis of complement components associated with the inflammatory syndrome in RA and masking a possibly increased catabolism (8,9 …”

“…The complement activation in RA is suggested by the finding of depressed levels and/or hemolytic activities of Cl, C4, C2, C3, properdin factor B, and properdin in synovial fluids (1,23). In the circulating blood, immune complexes have been demonstrated (4, 5) but an increased synthesis of certain complement components secondary to the inflammatory syndrome in RA often may mask a possible increase in their catabolism, therefore resulting in a normal or even augmented conventional complement profile (1,7,8). Indeed, with turnover studies, it was seen that complement was hypercatabolized not only in synovial fluid but also in blood from RA patients (9,10).…”