Publication: Histopathology and molecular pathology of synovial B-lymphocytes in rheumatoid arthritis
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Date
2000
Authors
Krenn, V. ; Souto-Carneiro, M. M. ; Kim, H.- J. ; Berek, C. ; Starostik, P. ; König, A. ; Harms, H. ; Müller-Hermelink, H. K.
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
B-cells of the rheumatoid synovial tissue are
a constant part of and, in some histopathological
subtypes, the dominant population of the inflammatory
infiltrate, located in the region of tissue destruction. The
pattern of B-cell distribution and the relationship to the
corresponding antigen-presenting cells (follicular
dendritic reticulum cells: FOCs) show a great variety. Bcells may exhibit (i) a follicular organization forming
secondary follicles; (ii) follicle-like patterns with
irregularly formed FOC networks, and (iii) a diffuse
pattern of isolated FOCs. Molecular analysis of
immunoglobulin YH and YL genes from human
synovial B-cell hybridomas and synovial tissue
demonstrates somatic mutations due to antigen
activation. The FOC formations in the synovial tissue
may therefore serve as an environment for B-cell
maturation, which is involved in the generation of
autoantibodies. An autoantibody is defined as
"pathogenic" if it fulfills the Witebsky-Rose-Koch
criteria for classical autoimmune diseases: definition of
the autoantibody; induction of the disease by transfer of
the autoantibody; and isolation of the autoantibody from
the disease-specific lesion. B-cells from rheumatoid
synovial tissue show specificity for FcIgG, type II
collagen, COMP, sONA, tetanus toxoid , mitochondrial
antigens (M2), filaggrin and bacterial HSPs. The
contributions of these antigens to the pathogenesis of RA
are still hypothetical. A possible contribution could
derive from crossreactivity and epitope mimicry: due to
crossreaction, an antibody directed originally against a
foreign infectious agent could react with epitopes from
articular tissues, perpetuating the local inflammatory
process. The characteristic distribution pattern, the
localisation within the area of tissue destruction, the
hypermutated IgYH and IgYL genes, and their exclusive
function to recognize conformation-dependent antigens
suggest a central role for B-cells in the inflammatory
Offprint requests to: Dr. Veit Krenn, MD., Institute for Pathology,
University of Wurzburg. Josef-Schneider-Str. 2, 0-97080 Wurzburg,
Germany. Fax: +49931 2013440. e-mail : path119@mail.uniwuerzburg.de
process of rheumatoid arthritis. Therefore, the analysis
of synovial B-cell hybridomas and experimental
expression of synovial IgYH and IgYL genes will help
to characterise the antigens responsible for the
pathogenesis of rheumatoid arthritis.
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Citation
Histology and Histopathology, Vol. 15, n.º 3 (2000)
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