Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Rheumatoid Arthritis: HELP
Retractions by Thomas W. J. Huizinga
Based on 302 articles published since 2009
(Why 302 articles?)
|||| 302 

Between 2009 and 2019, T. W. Huizinga wrote the following 2 articles about Arthritis, Rheumatoid.
+ Citations + Abstracts
1 Retraction Mast cells are the main interleukin 17-positive cells in anticitrullinated protein antibody-positive and -negative rheumatoid arthritis and osteoarthritis synovium. 2011

Suurmond, Jolien / Dorjée, Annemarie L / Boon, Mariëtte R / Knol, Edward F / Huizinga, Tom W J / Toes, René E M / Schuerwegh, Annemie J M. ·Department of Rheumatology, Leiden University Medical Center, PO Box 9600, Albinusdreef 2, C1-R, NL-2300 RC Leiden, The Netherlands. j.suurmond@lumc.nl ·Arthritis Res Ther · Pubmed #21933391.

ABSTRACT: INTRODUCTION: Mast cells have been implicated to play a functional role in arthritis, especially in autoantibody-positive disease. Among the cytokines involved in rheumatoid arthritis (RA), IL-17 is an important inflammatory mediator. Recent data suggest that the synovial mast cell is a main producer of IL-17, although T cells have also been implicated as prominent IL-17 producers as well. We aimed to identify IL-17 expression by mast cells and T cells in synovium of arthritis patients. METHODS: Synovial samples of anticitrullinated protein antibody-positive (ACPA+) and ACPA-negative (ACPA-) RA and osteoarthritis (OA) patients were stained for IL-17 in combination with CD117 (mast cells), CD3 (T cells) and CD68 (macrophages). Concentrations of IL-17 in synovial fluid were determined by ELISA. RESULTS: The number of IL-17+ cells in synovium was comparable in all groups. Although the vast majority of IL-17+ cells are mast cells, no difference in the percentage of IL-17+ mast cells was observed. Nonetheless, levels of IL-17 in synovial fluid were increased in ACPA+ RA patients compared to ACPA- RA and OA patients. CONCLUSIONS: The synovial mast cell is the main IL-17+ cell in all three arthritis groups analyzed. These data are relevant for studies aimed at blocking IL-17 in the treatment of arthritis.

2 Retraction Evidence for a functional role of IgE anticitrullinated protein antibodies in rheumatoid arthritis. 2010

Schuerwegh, A J M / Ioan-Facsinay, A / Dorjée, A L / Roos, J / Bajema, I M / van der Voort, E I H / Huizinga, T W J / Toes, R E M. ·Department of Rheumatology and Pathology, and Central Medical Immunology Laboratory, Leiden University Medical Center, Leiden 2300 RC, The Netherlands. a.j.m.schuerwegh@lumc.nl ·Proc Natl Acad Sci U S A · Pubmed #20133791.

ABSTRACT: Rheumatoid arthritis (RA) is a systemic autoimmune disease involving inflammation of the joints. Among the autoantibodies described in RA, anticitrullinated protein antibodies (ACPAs) are highly specific and predictive for RA. In addition, ACPAs have been implicated in the pathogenesis of RA. However, a direct functional response of immune cells from ACPA(+) RA patients toward citrullinated proteins has not been demonstrated. In this study, we show that exposure to citrullinated antigens leads to activation of basophils from ACPA(+) RA patients within 20 minutes. This was not observed after exposure of basophils to noncitrullinated control antigens or after stimulation of basophils from ACPA(-) RA patients and healthy controls. Basophil activation was correlated with the binding of citrullinated proteins to basophils. Furthermore, serum from ACPA(+) RA patients in contrast to that from ACPA(-) RA patients could specifically sensitize human FcepsilonRI expressing rat basophil cells (RBL), enabling activation by citrullinated proteins. Mast cell degranulation products such as histamine levels were enhanced in synovial fluid of ACPA(+) RA patients as compared with ACPA(-) RA and osteoarthritis patients. In addition, histamine levels in synovial fluid from ACPA(+) RA patients correlated with IgE levels, suggesting degranulation of mast cells by cross-linking IgE. Immunohistochemistry on synovial biopsies demonstrated an increased number of degranulated CD117(+) mast cells in ACPA(+) RA patients; IgE and FcepsilonRI expression in synovial mast cells from ACPA(+) RA patients was increased. In conclusion, our results show an immunological response of immune cells from ACPA(+) RA patients in a citrulline-specific manner. Moreover, these data indicate a role for IgE-ACPAs and FcepsilonRI-positive cells in the pathogenesis of RA.