Concise reports
Nuclear factor-
B activity in T cells from patients with
rheumatic diseases: A preliminary report
a Departamento
de Medicina, Rheumatology Unit, Hospital Universitario "Reina
Sofía", Spain, b Departamento de Fisiología e Inmunología, Facultad de
Medicina, Universidad de Córdoba, Spain
Correspondence to: Professor E Collantes-Estévez, Departamento de Medicina, Unidad de Reumatología. Facultad de Medicina, Avda Menéndez Pidal s/n, E-14071 Córdoba, Spain.
Accepted for publication 23 September 1998
OBJECTIVE
The NF-
B/Rel family of transcription
factors regulates the expression of many genes involved in the immune
or inflammatory response at the transcriptional level. The aim of this
study was to determine whether distinctive patterns of NF-kB activation are seen in different forms of joint disease.
METHODS
The DNA binding activity of these
nucleoproteins was examined in purified synovial and peripheral T cells
from patients with various chronic rheumatic diseases (12: four with
rheumatoid arthritis; five with spondyloarthropathies; and three with osteoarthritis).
RESULTS
Electrophoretic mobility shift assays
disclosed two specific complexes bound to a NF-
B specific
32P-labelled oligonucleotide in nucleoproteins extracted
from purified T cells isolated from synovial fluid and peripheral blood
of patients with rheumatoid arthritis. The complexes consisted of
p50/p50 homodimers and p50/p65 heterodimers. Increased NF-kB binding to DNA in synovial T cells was observed relative to peripheral T cells. In
non-rheumatoid arthritis, binding of NF-
B in synovial T cells was
exclusively mediated by p50/p50 homodimers.
CONCLUSION
Overall, the results suggest that
NF-
B may play a central part in the activation of infiltrating T
cells in chronic rheumatoid arthritis. The activation of this nuclear
factor is qualitatively different in rheumatoid synovial T cells to
that in other forms of non-rheumatoid arthritis (for example,
osteoarthritis, spondyloarthropathies).
B;
synovial T cells;
rheumatoid arthritis;
spondyloarthropathy;
osteoarthritis
© 1998 by Annals of the Rheumatic Diseases
This article has been cited by other articles:
-
Pattacini, L., Casali, B., Boiardi, L., Pipitone, N., Albertazzi, L., Salvarani, C.
(2007). Angiotensin II protects fibroblast-like synoviocytes from apoptosis via the AT1-NF-{kappa}B pathway. Rheumatology (Oxford)
46: 1252-1257
[Abstract] [Full Text] -
Remans, P. H. J., Gringhuis, S. I., van Laar, J. M., Sanders, M. E., Papendrecht-van der Voort, E. A. M., Zwartkruis, F. J. T., Levarht, E. W. N., Rosas, M., Coffer, P. J., Breedveld, F. C., Bos, J. L., Tak, P. P., Verweij, C. L., Reedquist, K. A.
(2004). Rap1 Signaling Is Required for Suppression of Ras-Generated Reactive Oxygen Species and Protection Against Oxidative Stress in T Lymphocytes. J. Immunol.
173: 920-931
[Abstract] [Full Text]
Register for free content
The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.
Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.
