| Abstract | Rheumatoid arthritis is an autoimmune disease which is characterized by chronic polyarthritis and joint destruction as well as by extra-articular manifestations, typically including the appearance of rheumatoid nodules. Although the pathogenesis of the disease is unknown, substantial evidence suggests that it is T cell-mediated. In contrast to experimental models, the disease-mediating T cells in the human situation have never been isolated or identified. We expanded T lymphocytes from human rheumatoid nodules by IL-2 stimulation and observed a marked oligoclonality among these expanded lymphocytes. This tendency towards oligoclonality was not seen in IL-2-expanded lymphocytes from peripheral blood. We hypothesize that this oligoclonal expansion reflects a clonally restricted in situ preactivation of lymphocytes and that precisely these preactivated cells are involved in the pathogenesis of the rheumatic process. |
| Authors | F De Keyser, G Verbruggen, E M Veys, C Cuvelier, A M Malfait, D Benoit, D Elewaut, J Vermeersch, A Heirwegh
(Affiliation: Department of Rheumatology, University Hospital, Ghent, Belgium.)
|
| Journal | Clinical immunology and immunopathology
(Clin Immunol Immunopathol)
Vol. 68
Issue 1
Pg. 29-34
(Jul 1993)
ISSN: 0090-1229 UNITED STATES |
| PMID | 8513590
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
| Chemical References |
- Antigens, CD4
- Antigens, CD8
- Immunoglobulin Variable Region
- Interleukin-2
- Receptors, Antigen, T-Cell, alpha-beta
|
| Topics |
- Aged
- Antigens, CD4
(analysis)
- Antigens, CD8
(analysis)
- Clone Cells
(immunology)
- Female
- Flow Cytometry
- Humans
- Immunoglobulin Variable Region
(metabolism)
- Immunohistochemistry
- Interleukin-2
(pharmacology)
- Lymphocytes
(drug effects, immunology, ultrastructure)
- Male
- Middle Aged
- Receptors, Antigen, T-Cell, alpha-beta
(analysis)
- Rheumatoid Nodule
(pathology)
- T-Lymphocytes
(cytology)
|
