The pathogenic role of rheumatoid factor in rheumatoid arthritis

2010 ◽  
Vol 5 (6) ◽  
pp. 651-658 ◽  
Author(s):  
Yeong Wook Song ◽  
Eun Ha Kang
Keyword(s):  
Rheumatoid Arthritis ◽  
Rheumatoid Factor ◽  
Pathogenic Role

scholarly journals Activation of CD16+ effector cells by rheumatoid factor complex. Role of natural killer cells in rheumatoid arthritis

1991 ◽  
Vol 34 (4) ◽  
pp. 423-431 ◽  
Author(s):  
Christian Hendrich ◽  
Jens G. Kuipers ◽  
Waldemar Kolanus ◽  
Reinhold E. Schmidt ◽  
Michael Hammer
Keyword(s):  
Rheumatoid Arthritis ◽  
Natural Killer Cells ◽  
Rheumatoid Factor ◽  
Natural Killer ◽  
Killer Cells ◽  
Effector Cells

AB0154 Pathogenic Role of Irhom2 in Seropositive Rheumatoid Arthritis

2014 ◽  
Vol 73 (Suppl 2) ◽  
pp. 854.2-854
Author(s):  
Y.J. Kim ◽  
E.-J. Lee ◽  
S. Hong ◽  
B.S. Koo ◽  
W.J. Seo ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Pathogenic Role ◽  
Seropositive Rheumatoid Arthritis

scholarly journals Pathogenic role of CXCR7 in rheumatoid arthritis

2010 ◽  
Vol 62 (11) ◽  
pp. 3211-3220 ◽  
Author(s):  
Kaori Watanabe ◽  
Mark E. T. Penfold ◽  
Akio Matsuda ◽  
Naho Ohyanagi ◽  
Kayoko Kaneko ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Pathogenic Role

scholarly journals Historical observations contributing insights on etiopathogenesis of rheumatoid arthritis and role of rheumatoid factor

2016 ◽  
Vol 213 (10) ◽  
pp. 1937-1950 ◽  
Author(s):  
Eng M. Tan ◽  
Josef S. Smolen
Keyword(s):  
Rheumatoid Arthritis ◽  
Rheumatoid Factor ◽  
Inflammatory Mediators ◽  
Targeting Therapy ◽  
Initiation Phase ◽  
Novel Approach ◽  
Recurrent Inflammation ◽  
Antigen Antibody ◽  
Second Wave

When studies on rheumatoid arthritis (RA) that were made many decades ago and could be considered “historical” in nature are analyzed in the context of recent observations, important insights on RA and on the function of rheumatoid factor (RF) become apparent. RF in the role of antibody to immune complexes (ICs) appears to be involved in activation of the complement system and in the production of chemotactic and inflammatory mediators, creating a condition that can be sustained and reinitiated. In the synovial cavity, a state of nonresolving inflammation is produced with the formation of citrullinated protein antigen–antibody complexes or other forms of ICs. This is followed by a second wave of IC production in the form of RF acting as antibody reactive with the initial ICs. Both of these processes are associated with complement consumption and production of inflammatory mediators. We present a model of an initiation phase of RA that might represent an example of repetitive formation of ICs and complement-mediated inflammation. Targeting therapy at this phase of RA to break the cycles of recurrent inflammation might be a novel approach to aid in further control of the disease.

scholarly journals Pathological Role of Interleukin-6 in Psoriatic Arthritis

Arthritis ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Atsushi Ogata ◽  
Atsushi Kumanogoh ◽  
Toshio Tanaka
Keyword(s):  
Rheumatoid Arthritis ◽  
Psoriatic Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Pathogenic Role ◽  
Psoriatic Disease ◽  
Effector Phase ◽  
Priming Phase ◽  
Necrosis Factor

Psoriatic arthritis (PsA) is a clinical manifestation of psoriatic disease. Although the pathogenesis of PsA remains unknown, PsA can be managed by treatments similar to those used for rheumatoid arthritis (RA). Because interleukin-(IL-) 6 has been suggested to have a pathogenic role in PsA, a humanized anti-IL-6 receptor antibody tocilizumab treatment for PsA was recently tried. However, the efficacy of tocilizumab for PsA was not favorable. This suggests that the pathogenic roles of IL-6 in PsA and RA are different. In RA, tumor necrosis factor (TNF) primarily contributes to the arthritis effector phase and IL-6 contributes to the arthritis priming phase. In PsA, the TNF-related effector phase is similar to that in RA, but the IL-6-related priming phase might not be critical. This paper discusses the role of IL-6 in PsA.

scholarly journals Rheumatoid factor: a cause of fals positive histoplasmin latex agglutination

1977 ◽  
Vol 5 (1) ◽  
pp. 31-33
Author(s):  
R W Oxenhandler ◽  
E H Adelstein ◽  
W A Rogers
Keyword(s):  
Rheumatoid Arthritis ◽  
Rheumatoid Factor ◽  
False Positive ◽  
Complement Fixation ◽  
High Titer ◽  
Latex Agglutination ◽  
Immunoglobulin M ◽  
Cold Agglutinins ◽  
Clinical Records

Ten of thirteen patients with positive histolatex agglutination titers of 1:32 or greater had no evidence of acute histoplasmosis.Three of these false positives had rheumatoid arthritis. A fourth had a rising mycoplasma complement fixation titer, and the fifth had a high titer of cold agglutinins. All of these are associated with abnormal immunoglobulin M production. To evaluate the role of rheumatoid factor in producing false positive histolatex agglutination, the histolatex test was performed on sera from 32 patients having rheumatoid factor at a titer of 1:40 or greater. Four of these sera agglutinated the histoplasmin-coated latex particles at titers of 1:32 or greater. Review of clinical records suggests the this reactivity is nonspecific. It is our purpose to call attention to rheumatoic factor as a cause of false positive histolatex agglutination.

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