Functional characterization of SV40-transformed adherent synovial cells from rheumatoid arthritis

Author:

GOTO M123,OKAMOTO M3,SASANO M3,NISHIZAWA K3,AOTSUKA S4,YAMAGUCHI N5,OBINATA M6,IKEDA K7

Affiliation:

1. Division of Rheumatic Diseases, Tokyo Metropolitan Otsuka Hospital

2. Department of Medicine and Physical Therapy, University of Tokyo

3. Institute of Rheumatology, Tokyo Women's Medical College

4. Division of Clinical Immunology. National Clinical Center

5. Institute of Medical Science, University of Tokyo

6. Institute of Mycobacteria Research, Tohoku University

7. Department of Ultrastructure, Psychiatric Research Institute of Tokyo, Japan

Abstract

SUMMARY A total of 14 transformed cell clones were obtained by micro-injecting origin-defective SV40 DNA into three types of cloned adherent synovial cells (ASC) (dendritic cells (DCs), macrophage-Iike cells (MCs), and fibroblast-like cells (FCs)) from two rheumatoid arthritis patients (five DC clones (SV40-DCs), five MC clones (SV40-MCs) and four FC clones (SV40-FCs)). All the transformed cell nuclei expressed SV40-specific T antigen. The cells which formed a colony had a few times shorter doubling time than the original cells. IL-1α, IL-lβ and prostaglandin E2 were detected in the culture supernatant from the unstimulated transformed cells like untransformed cells. The SV40-DCs showed the most potent accessory cell function in oxidative mitogenesis assay among the three types of SV40-ASCs. Granulocyte macrophage colony stimulatory factor (GM-CSF) was detected only in the culture supernatant from the SV40-MCs without stimulation. Extensive phenotypic analysis revealed relatively cell-specific markers. SV40-DCs were HLA-DP+ and glial fibrillary acidic protein positive. SV40-MCs stained positive for 5′-nucleotidase and nonspecific esterase. These transformed ASCs retained much of the original cellular physiology of rheumatoid arthritis (RA) ASCs and may be a useful tool for characterizing the role of ASCs in the pathogenesis of RA.

Publisher

Oxford University Press (OUP)

Subject

Immunology,Immunology and Allergy

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