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Analysis of the cellular infiltrates and expression of cytokines in synovial tissue from patients with rheumatoid arthritis and reactive arthritis
Author(s) -
Smeets Tom J. M.,
Dolhain Radboud J. E. M.,
Breedveld Ferdinand C.,
Tak Paul P.
Publication year - 1998
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199809)186:1<75::aid-path142>3.0.co;2-b
Subject(s) - rheumatoid arthritis , granzyme b , medicine , granzyme , inflammation , immunology , arthritis , immune system , cd38 , synovitis , cytokine , interferon gamma , infiltration (hvac) , synovial membrane , pathology , cd8 , biology , cd34 , stem cell , physics , perforin , genetics , thermodynamics
The cellular infiltrates and cytokine patterns in synovial tissue (ST) from patients with rheumatoid arthritis (RA) and reactive arthritis (ReA) were compared in order to determine the mechanisms responsible for the chronic and destructive course of RA. Since the results could be influenced by differences in disease duration, ST was studied from patients in both early and late stages of the disease. Ten patients had early RA (<1 year), ten long‐standing RA (>1 year), six early ReA (<1 year), and five long‐standing ReA (>1 year). Histological analysis demonstrated that the scores for infiltration by lymphocytes and plasma cells, and the scores for inflammation, were significantly higher in RA than in ReA. Immunolabelling studies showed that in particular, the scores for infiltration by CD38+ plasma cells, granzyme B+ cells, and interferon‐gamma (IFNγ)+ cells were significantly higher in RA than in ReA. The results were independent of the disease duration. The increased number of lymphocytes, plasma cells, and granzyme B+ cells in rheumatoid synovial tissue supports the paradigm that RA is the result of specific immune recognition in the joint and that granzyme B+ cells play an important role in joint destruction. © 1998 John Wiley & Sons, Ltd.