EXPRESSION OF L-SELECTIN, CD43, AND CD44 IN SYNOVIAL-FLUID NEUTROPHILS FROM PATIENTS WITH INFLAMMATORY JOINT DISEASES - EVIDENCE FOR A SOLUBLE FORM OF L-SELECTIN IN SYNOVIAL-FLUID

Citation
A. Humbria et al., EXPRESSION OF L-SELECTIN, CD43, AND CD44 IN SYNOVIAL-FLUID NEUTROPHILS FROM PATIENTS WITH INFLAMMATORY JOINT DISEASES - EVIDENCE FOR A SOLUBLE FORM OF L-SELECTIN IN SYNOVIAL-FLUID, Arthritis and rheumatism, 37(3), 1994, pp. 342-348
Citations number
34
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
00043591
Volume
37
Issue
3
Year of publication
1994
Pages
342 - 348
Database
ISI
SICI code
0004-3591(1994)37:3<342:EOLCAC>2.0.ZU;2-X
Abstract
Objective. To study the expression of L-selectin, CD43, and CD44 on pe ripheral blood (PB) and synovial fluid (SF) neutrophils from patients with inflammatory joint diseases, and to investigate the presence of s oluble L-selectin in both Sr and plasma from patients with acute and c hronic arthritis. Methods. PB and SF neutrophils were isolated from 13 patients with rheumatoid arthritis (RA) and 17 patients with various inflammatory joint diseases other than RA. Expression of L-selectin, C D43, CD44, CD11a, and CD11b was determined in both unstimulated and in vitro-activated cells by immunofluorescence flow cytometry. Soluble L -selectin levels were estimated in Sr and plasma by a semiquantitative radioimmunoassay. Results. Neutrophils from SF showed diminished expr ession of L-selectin compared with PB neutrophils; CD43 expression and CD44 expression were decreased in SF neutrophils from most patients. In contrast, SF neutrophils exhibited significantly increased expressi on of CD11b, to an extent similar to that seen with in vitro-activated PB neutrophils. Soluble L-selectin was detected at similar levels in Sr and PB. Conclusion. The phenotypic profile of Sr neutrophils (low l evels of L-selectin, CD43, and CD44, and high levels of CD11b) from mo st patients with RA or other inflammatory joint conditions resembles t hat observed in in vitro-activated neutrophils. Our results suggest th at SF neutrophils are activated to a similar degree in inflammatory jo int diseases with different pathogenic mechanisms.