Objective. To investigate synovial fluid (SF) for the presence of CR1
and to study its relationship to SF leukocytes and to serum levels of
soluble CR1 (sCR1) in patients with rheumatic diseases. Methods. Synov
ial fluids were collected from 35 patients with rheumatoid arthritis (
RA) and 26 patients with other inflammatory joint diseases, Total CR1
in the SF and serum were measured with a sandwich enzyme-linked immuno
sorbent assay (ELISA) that recognized both soluble and transmembrane f
orms of CR1, The characteristics of CR1 in SF were analyzed by ultrace
ntrifugation and by a second ELISA specific for transmembrane CR1. Res
ults. CR1 was found in all SF samples tested (range 5-281 ng/ml), SF C
R1 was higher in patients with RA (mean +/- SD 81 +/- 66 ng/ml) than i
n those with other inflammatory joint diseases (31.8 +/- 23.8 ng/ml) (
P < 0.001), Serum sCR1 was not significantly increased in the patients
compared with the normal subjects, There was no correlation between s
erum sCR1 and SF CR1, In 14% of the patients, the SF CR1 level was hig
her than the serum sCR1 level, A fraction (30-80%) of SF CR1 was pelle
ted by ultracentrifugation and, unlike serum sCR1, it reacted in an EL
ISA specific for transmembrane CR1, Thus, SF contained 2 forms of CR1:
a membrane-associated and a soluble form, which was confirmed by sucr
ose density-gradient ultracentrifugation, SF CR1 levels correlated dir
ectly with the number of SF total leukocytes and polymorphonuclear leu
kocytes (PMN). These 2 forms of CR1 were also found in the supernatant
of in vitro-activated PMN from normal subjects, SF CRI exhibited the
capacity to act as a cofactor for the factor I degradation of C3b. Con
clusion. CR1 is found in the SF of patients with joint inflammation, T
he data suggest that SF CR1 originates from the infiltrating leukocyte
s, which shed both a soluble and a membrane-associated form, Whether S
F CR1 participates in the local regulation of complement activation re
mains to be examined.