| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS | REGISTER |
|
|
|
|
|||||||||||||
|
|
|||||||||||||||
receptors
Department of
Medicine, Unit of Rheumatology, Karolinska Institute, Stockholm, Sweden
Correspondence to: Drs L Berg and J Lampa, Department of Medicine, Unit of Rheumatology, Karolinska Hospital, CMM L8:04, 171 76 Stockholm, Sweden louise.berg{at}cmm.ki.se jon.lampa{at}divmed.ks.se
Accepted for publication 28 June 2000
OBJECTIVE
Peripheral T
cells from patients with rheumatoid arthritis (RA) are hyporesponsive
when stimulated with antigen or mitogen in vitro, possibly owing to
increased production of proinflammatory cytokines such as tumour
necrosis factor 
(TNF). This study sought to find out if and how
RA T cell reactivity is affected during treatment with etanercept
(Enbrel), a soluble TNF receptor.
METHODSHeparinised
blood was collected from patients with RA at baseline, after four and
eight weeks of etanercept treatment, and from healthy controls. After
density separation spontaneous production of interferon 
(IFN),
TNF, interleukin 6 (IL6), and IL10 by peripheral blood mononuclear
cells (PBMC) was detected by ELISPOT. For detection of T cell
reactivity, PBMC were stimulated in vitro with mitogen
(phytohaemagglutinin (PHA)), microbial antigens (purified protein
derivative (PPD), influenza), or an autoantigen, collagen type II
(CII). Supernatants were analysed for IFN and IL2 content by enzyme
linked immunosorbent assay (ELISA).
RESULTSIn RA the
number of cells spontaneously producing IFN was significantly
increased after four, but not eight weeks' treatment with etanercept.
T cell reactivity, as measured by IFN production to PPD, influenza,
and CII was significantly increased after four and sustained after
eight weeks' treatment, whereas IFN production induced by PHA
remained unchanged. TNF production was significantly higher in
patients with RA than in controls and did not change during etanercept treatment.
CONCLUSIONTreatment
of patients with RA with etanercept may lead to increased peripheral T
cell reactivity both to microbial antigens and to self antigens such as
CII. These findings indicate that TNF blockade may not only suppress
but also stimulate certain aspects of antimicrobial immune defence and autoimmunity.
This article has been cited by other articles:
|
|
 |
|
  M Dastmalchi, C Grundtman, H Alexanderson, C P Mavragani, H Einarsdottir, S B. Helmers, K Elvin, M K Crow, I Nennesmo, and I E Lundberg A high incidence of disease flares in an open pilot study of infliximab in patients with refractory inflammatory myopathies Ann Rheum Dis, December 1, 2008; 67(12): 1670 - 1677. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Sellam, H. Hamdi, C. Roy, G. Baron, M. Lemann, X. Puechal, M. Breban, F. Berenbaum, M. Humbert, K. Weldingh, et al. Comparison of in vitro-specific blood tests with tuberculin skin test for diagnosis of latent tuberculosis before anti-TNF therapy Ann Rheum Dis, December 1, 2007; 66(12): 1610 - 1615. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. T H Jacobsson, C. Turesson, J.-A. Nilsson, I. F Petersson, E. Lindqvist, T. Saxne, and P. Geborek Treatment with TNF blockers and mortality risk in patients with rheumatoid arthritis Ann Rheum Dis, May 1, 2007; 66(5): 670 - 675. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. H. Roux, O. Brocq, V. Breuil, C. Albert, and L. Euller-Ziegler Safety of anti-TNF-{alpha} therapy in rheumatoid arthritis and spondylarthropathies with concurrent B or C chronic hepatitis Rheumatology, October 1, 2006; 45(10): 1294 - 1297. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M Andersson, E Svenungsson, M Khademi, J Lampa, L Brundin, and E Wallstrom No signs of immunoactivation in the cerebrospinal fluid during treatment with infliximab Ann Rheum Dis, September 1, 2006; 65(9): 1237 - 1240. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J Clark, P Vagenas, M Panesar, and A P Cope What does tumour necrosis factor excess do to the immune system long term? Ann Rheum Dis, November 1, 2005; 64(suppl_4): iv70 - iv76. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L H Calabrese, N Zein, and D Vassilopoulos Safety of antitumour necrosis factor (anti-TNF) therapy in patients with chronic viral infections: hepatitis C, hepatitis B, and HIV infection Ann Rheum Dis, November 1, 2004; 63(suppl_2): ii18 - ii24. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Schotte, B. Schluter, P. Willeke, E. Mickholz, M. A. Schorat, W. Domschke, and M. Gaubitz Long-term treatment with etanercept significantly reduces the number of proinflammatory cytokine-secreting peripheral blood mononuclear cells in patients with rheumatoid arthritis Rheumatology, August 1, 2004; 43(8): 960 - 964. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R Nissinen, M Leirisalo-Repo, R Peltomaa, T Palosuo, and O Vaarala Cytokine and chemokine receptor profile of peripheral blood mononuclear cells during treatment with infliximab in patients with active rheumatoid arthritis Ann Rheum Dis, June 1, 2004; 63(6): 681 - 687. [Abstract] [Full Text]
|
|
|
|
|
|
J Zou, M Rudwaleit, J Brandt, A Thiel, J Braun, and J Sieper Up regulation of the production of tumour necrosis factor {alpha} and interferon {gamma} by T cells in ankylosing spondylitis during treatment with etanercept Ann Rheum Dis, June 1, 2003; 62(6): 561 - 564. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. P. Cope Exploring the reciprocal relationship between immunity and inflammation in chronic inflammatory arthritis Rheumatology, June 1, 2003; 42(6): 716 - 731. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O Kaipiainen-Seppanen and M Leino Recurrent uveitis in a patient with juvenile spondyloarthropathy associated with tumour necrosis factor {alpha} inhibitors Ann Rheum Dis, January 1, 2003; 62(1): 88 - 89. [Full Text] [PDF]
|
|
|
|
 |
|
 V. P. Werth and A. I. Levinson Etanercept-Induced Injection Site Reactions: Mechanistic Insights From Clinical Findings and Immunohistochemistry Arch Dermatol, July 1, 2001; 137(7): 953 - 955. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS | REGISTER |
