Article
Arguments for interleukin 1 as a target in chronic arthritis
Wim B van den Berg
Department of
Rheumatology, University Medical Centre St Radboud, Nijmegen, the
Netherlands
Correspondence to: Dr van den Berg, Rheumatology Research Laboratory, University Medical Centre St Radboud, 6500 HB Nijmegen, the Netherlands (w.vandenberg{at}reuma.azn.nl)
Tumour necrosis factor (TNF) and interleukin 1 (IL1) are
considered as master cytokines in chronic, destructive arthritis. Therapeutic approaches in rheumatic arthritis (RA) patients so far
mainly focused on TNF. Although TNF is a major inflammatory mediator in
RA and a potent inducer of IL1, anti-TNF treatment is not effective in
all patients, nor does it fully control the arthritic process in
affected joints of good responders. Analysis of cytokine patterns in
early synovial biopsy specimens of RA patients reveals prominent TNF
staining in 50% of the patients, whereas IL1b staining was evident in
100%. This argues that TNF independent IL1 production occurs in some
of the patients. Studies in a range of experimental arthritis models in
mice make it clear that TNF is involved in early joint swelling.
However, TNF alone is not arthritogenic nor destructive and exerts its
arthritogenic potential through IL1 induction. Intriguingly, TNF
independent IL1 production is found in many models. Its relevance is
further underlined by the greater efficacy of anti-IL1 treatment as
compared with anti-TNF treatment and the total lack of chronic, erosive arthritis in IL1b deficient mice. IL1b is not necessarily involved in
early joint swelling, but is a crucial mediator in chronic arthritis
and cartilage erosion in all models studied so far. This makes ILb an
attractive target in chronic, destructive arthritis.
© 2000 by Annals of the Rheumatic Diseases
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
-
Zheng, B., Marinova, E., Switzer, K., Wansley, D., He, H., Bheekha-Escura, R., Behrens, T. W., Han, S.
(2007). Overexpression of BclXL in B Cells Promotes Th1 Response and Exacerbates Collagen-Induced Arthritis. J. Immunol.
179: 7087-7092
[Abstract] [Full Text]
- Full Text
- Full Text (PDF)
- Submit a response
- Alert me when this article is cited
- Alert me when eLetters are posted
- Alert me if a correction is posted
- Citation Map
Services
- Email this link to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Add article to my folders
- Download to citation manager
- Request Permissions
Citing Articles
Google Scholar
PubMed
Bookmark with
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.
