title: CR1, CD35 in synovial fluid from patients with inflammatory joint diseases.
abstract: 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
  Synovial 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 immunosorbent assay (ELISA) that recognized both soluble and transmembrane forms of CR1. The characteristics of CR1 in SF were analyzed by ultracentrifugation and by a second ELISA specific for transmembrane CR1.
  
  
  RESULTS
  CR1 was found in all SF samples tested (range 5-281 ng/ml). SF CR1 was higher in patients with RA (mean +/- SD 81 +/- 66 ng/ml) than in 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 serum sCR1 and SF CR1. In 44% of the patients, the SF CR1 level was higher than the serum sCR1 level. A fraction (30-80%) of SF CR1 was pelleted by ultracentrifugation and, unlike serum sCR1, it reacted in an ELISA specific for transmembrane CR1. Thus, SF contained 2 forms of CR1: a membrane-associated and a soluble form, which was confirmed by sucrose density-gradient ultracentrifugation. SF CR1 levels correlated directly with the number of SF total leukocytes and polymorphonuclear leukocytes (PMN). These 2 forms of CR1 were also found in the supernatant of in vitro-activated PMN from normal subjects. SF CR1 exhibited the capacity to act as a cofactor for the factor I degradation of C3b.
  
  
  CONCLUSIONS
  CR1 is found in the SF of patients with joint inflammation. The data suggest that SF CR1 originates from the infiltrating leukocytes, which shed both a soluble and a membrane-associated form. Whether SF CR1 participates in the local regulation of complement activation remains to be examined.
authors.affiliation: University Hospital, Basel, Switzerland.
authors.forename: S
authors.initials: S
authors.lastname: Sadallah
authors.forename: E
authors.initials: E
authors.lastname: Lach
authors.forename: H U
authors.initials: HU
authors.lastname: Lutz
authors.forename: S
authors.initials: S
authors.lastname: Schwarz
authors.forename: P A
authors.initials: PA
authors.lastname: Guerne
authors.forename: J A
authors.initials: JA
authors.lastname: Schifferli
mesh_terms: D001168:Arthritis / Q000097:blood / Q000378:metabolism*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000378:metabolism; D002499:Centrifugation, Density Gradient / Q000379:methods; D004591:Electrophoresis, Polyacrylamide Gel / Q000379:methods; D006801:Humans; D015151:Immunoblotting; D009504:Neutrophils / Q000378:metabolism; D010003:Osteoarthritis / Q000097:blood / Q000378:metabolism; D011951:Receptors, Complement / Q000032:analysis* / Q000097:blood; D012967:Sodium Dodecyl Sulfate; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000378:metabolism; D013395:Sucrose; D013582:Synovial Fluid / Q000737:chemistry*; D014461:Ultracentrifugation
chemical_list: D011951:Receptors, Complement; D012967:Sodium Dodecyl Sulfate; D013395:Sucrose