PMID- 17786135
OWN - NLM
STAT- MEDLINE
DCOM- 20070913
LR  - 20161021
IS  - 1732-2693 (Electronic)
IS  - 0032-5449 (Linking)
VI  - 61
DP  - 2007 Aug 28
TI  - [Autoimmune aspects of treatment with TNF-alpha inhibitors].
PG  - 478-84
AB  - Tumor necrosis factor-alpha (TNF-alpha) plays an important role in the 
      pathogenesis of such diseases as rheumatoid arthritis, Crohn's disease, 
      ankylosing spondylitis, psoriatic arthritis, and juvenile chronic arthritis. 
      Recent years have brought improvement in the understanding of the pathogeneses of 
      these diseases, resulting in the production of new groups of biological drugs, 
      including, among others, anti-TNF-alpha antibodies. The use of TNF inhibitors has 
      been a great advance in the treatment of patients with these inflammatory 
      diseases. Infliximab and adalimumab are monoclonal antibodies that bind to and 
      neutralize the activity of TNF-alpha. Infliximab is a mouse/human chimera that 
      joins the variable regions of a mouse antibody to the constant region of human 
      IgG1. Adalimumab is a fully human IgG1 antibody. Etanercept is a dimeric fusion 
      protein that joins the human p75 TNF receptor to the Fc domain of human IgG1. The 
      beneficial effects of the anti-TNF monoclonal antibodies infliximab and 
      adalimumab and the soluble receptor fusion protein etanercept in the treatment of 
      rheumatoid arthritis, especially in patients resistant to other disease-modifying 
      antirheumatic drugs (DMARDs), are discussed. We observe stoppage of articular 
      destruction during treatment with TNF-alpha inhibitors. Soon after the 
      introduction of this therapy it was found that these agents have a propensity for 
      stimulating the production of autoantibodies and antibodies against themselves. 
      In this review, recent studies analyzing the effect of TNF-alpha blockade 
      (infliximab, etanercept, and adalimumab) on the ANA, anti-dsDNA, and 
      anticardiolipin antibody profiles in autoimmune diseases are discussed.
FAU - Kolarz, Bogdan
AU  - Kolarz B
AD  - Katedra i Klinika Reumatologii i Ukladowych Chorob Tkanki Lacznej Akademii 
      Medycznej im. prof. F. Skubiszewskiego w Lublinie, Lublin, Poland. 
      maria.majdan@am.lublin.pl
FAU - Targonska-Stepniak, Bozena
AU  - Targonska-Stepniak B
FAU - Darmochwal-Kolarz, Dorota
AU  - Darmochwal-Kolarz D
FAU - Majdan, Maria
AU  - Majdan M
LA  - pol
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Autoimmunizacja w trakcie terapii biologicznej z zastosowaniem antagonistow TNF.
DEP - 20070828
PL  - Poland
TA  - Postepy Hig Med Dosw (Online)
JT  - Postepy higieny i medycyny doswiadczalnej (Online)
JID - 101206517
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - B72HH48FLU (Infliximab)
RN  - FYS6T7F842 (Adalimumab)
SB  - IM
MH  - Adalimumab
MH  - Antibodies, Monoclonal/therapeutic use
MH  - Antibodies, Monoclonal, Humanized
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Juvenile/drug therapy
MH  - Arthritis, Psoriatic/drug therapy
MH  - Arthritis, Rheumatoid/drug therapy
MH  - Crohn Disease/drug therapy
MH  - Humans
MH  - Infliximab
MH  - Receptors, Tumor Necrosis Factor/*therapeutic use
MH  - Rheumatic Diseases/*drug therapy/immunology
MH  - Spondylitis, Ankylosing/drug therapy
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
RF  - 42
EDAT- 2007/09/06 09:00
MHDA- 2007/09/14 09:00
CRDT- 2007/09/06 09:00
PHST- 2007/08/13 00:00 [accepted]
PHST- 2007/06/15 00:00 [received]
PHST- 2007/09/06 09:00 [pubmed]
PHST- 2007/09/14 09:00 [medline]
PHST- 2007/09/06 09:00 [entrez]
AID - 498159 [pii]
PST - epublish
SO  - Postepy Hig Med Dosw (Online). 2007 Aug 28;61:478-84.