- Author:
Kwang Pyo HONG
1
;
In Hong CHOI
;
Gye Sung KIM
;
Bong Ki LEE
;
Jung Koo YOUN
;
Byeong Mun PARK
Author Information
- Publication Type:Original Article
- Keywords: Rheumatoid arthritis; NK; ADCC; LIF; Immune complex
- MeSH: Adult; Antibody-Dependent Cell Cytotoxicity; Antigen-Antibody Complex/immunology; Arthritis, Rheumatoid/immunology*; Female; Human; Killer Cells, Natural/immunology; Leukocyte Migration-Inhibitory Factors/biosynthesis; Male; Middle Age; Synovial Fluid/immunology
- From:Yonsei Medical Journal 1987;28(2):98-104
- CountryRepublic of Korea
- Language:English
- Abstract: Nonspecific immune parameters such as natural killer(NK) activity, antibody-dependent cellular cytotoxicity(ADCC), production of leukocyte migration inhibitory factor(LlF) and levels of immune complex(IC) were assessed in 47 patients with rheumatoid arthritis (RA) 20 with degenerative arthritis (DA) and 40 healthy controls. Peripheral blood (PB) as well as synovial fluid (SF) were collected from both RA and DA patients before treatment. Mononuclear cell suspensions and sera were prepared and submitted for the in vitro tests; 4-hr chromium-release assays using human K562 and mouse L1210 cells as targets for NK and ADCC assays respectively, 2-step agarose assay for LIF and platelet aggregation test for IC. Results revealed that 1) LIF activity of PB lymphocytes (PBL) from both RA and DA patients showed a significant (P < 0.05) decrease as compared with that from healthy controls. 2) PB-NK activity from RA patients showed an insignificant decrease as compared with that from DA or healthy controls. However, mononuclear cells isolated from SF (SFL) of RA patients exhibited significantly(P < 0.02) lower NK activity than PBL from the same patients. 3) In ADCC assays with PBL no significant differencies were observed among the 3 groups. 4) Higher titers of IC were detected in both PB and SF from RA patients than DA, and a negative correlation was found between serum IC levels and PB-NK activity. These data are discussed in light of previous reports, and a hypothesis regarding a decreased nonspecific cell-mediated immunity in conjunction with an increased humoral immune response, particularly in local sites, is proposed as one of the mechanisms underlying the pathogenesis of RA.