Open AccessImmunopathological features of palatine tonsil characteristic of IgA nephropathy: IgA1 localization in follicular dendritic cells
Author(s) -
KUSAKARI C.,
NOSE M.,
TAKASAKA T.,
YUASA R.,
KATO M.,
MIYAZONOU K.,
FUJITAIJ T.,
KYOGOKU M.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06012.x
Subject(s) - palatine tonsil , tonsil , nephropathy , immunology , follicular dendritic cells , medicine , pathology , biology , immune system , antigen presenting cell , t cell , diabetes mellitus , endocrinology
SUMMARY IgA nephropathy (IgAN) is generally thought to be mediated by the glomerular deposition of circulating immune complexes containing IgA as the major antibody component. Upper respiratory infections and tonsillitis often precede IgAN. and in some cases tonsillectomy is affective for the (treatment of IgAN. Thus, the tonsil seems to be a unique organ causing initial and/or progressive events to generate nephritogenic immune complexes in IgAN. in this study we focused on the analysis of immunopathological features of the palatine tonsil characteristic of IgAN patients by using an immunohistochemical technique. The IgAl subclass was demonstrated in follicular dendritic cells (FDC) of the tonsil of IgAN patients, but not in FDC of non‐IgAN controls. On the other hand, IgA2, IgG, IgM and C3 did not show any differences in distribution between the two groups. Moreover, the expression of decay‐accelerating factor (DAF), an inhibitor of homologous complement activation, and transforming growth factor‐beta I (TGF‐/β1). an inducer of antibody‐producing ceils to IgA class switching, in FDC and interdigitating dendritic cells of the tonsil, respectively, which was also clarified in this study for the first time, was found to be identically distributed in the two groups. These findings may support the idea that IgA1. possibly in an immune complex form, is trapped by FDC and plays an important role in the persistent activation of particular B cell repertoires responsible for ihe onset and/or progression of IgAN.