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Query: UMLS:C0039483 (
giant cell arteritis
)
3,204
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To determine the phenotype of infiltrating mononuclear cells in patients with
temporal arteritis
(TA), we performed immunohistochemical studies on temporal artery biopsy specimens from 24 patients with biopsy-proven TA. Interdigitating reticulum cells (IRC) were observed in 41% of the patients; disease duration was significantly shorter in these patients than in patients lacking IRC (mean 1.5 months versus 3.8 months). Infiltrating cells consisted predominantly of HLA-DR-expressing macrophages and T lymphocytes, especially of the CD4 subset. There were few B cells and no K cells. No relationship between cellular distribution and disease duration or treatment was found. Interleukin-2 receptor expression was observed in 87.5% of biopsy specimens obtained prior to or within the first 4 days of treatment with prednisone, but in only 14% of specimens obtained later. The presence of IRC in patients with TA suggests an autoimmune reaction directed against an antigenic substance that resides in the arterial wall and is presented and processed in situ. DR-expressing macrophages activated by CD4+ T lymphocytes may contribute to arterial damage in TA. Corticosteroids do not modify cellular distribution but induce important functional changes, as demonstrated by the disappearance of
interleukin-2 receptor
expression in patients treated for more than 4 days.
...
PMID:Immunohistochemical analysis of lymphoid and macrophage cell subsets and their immunologic activation markers in temporal arteritis. Influence of corticosteroid treatment. 278 41
Giant cell vasculitis is an arteritis that predominantly affects medium- and large-sized arteries. Genetic risk factors and clonal expansion of selected CD4+ T cell specificities in the vascular lesions support the model that
giant cell arteritis
is a T-cell-driven disease. Interferon (IFN)-gamma production in the tissue is intimately associated with the formation of the inflammatory infiltrates. Antigens inducing stimulation of T cells are unknown. To provide indirect evidence for the type and the tissue localization of the antigen, we examined CD4+ T cells in the lesions that secrete IFN-gamma. Temporal artery specimens from patients with
giant cell arteritis
were analyzed bu two-color immunohistochemistry applying antibodies to T cell markers. IFN-gamma, the
interleukin-2 receptor
alpha-chain (CD25) and talin, a cytoskeletal protein that is reorganized in T cells interacting with antigen-presenting cells. Proliferating cells in the lesions were identified through the expression of the Ki-67 nuclear antigen. More than 90% of tissue-infiltrating IFN-gamma-producing cells were CD4+ CD45RO+. They represented a minute subset (2 to 4%) of tissue-infiltrating T cells. IFN-gamma+ T cells aggregated in the adventitial layer of the inflamed artery where they were either diffusely distributed or arranged in clusters. The majority of IFN-gamma-secreting T cells expressed CD25. IFN-gamma+ T cells included a fraction of cells that had reorganized the cytoskeletal protein talin, indicating an interaction of the T cell receptor and an antigen-presenting cell. A subset of IFN-gamma-expressing T cells was undergoing proliferation in the tissue. IFN-gamma-producing T cells in vasculitic lesions of
giant cell arteritis
express several markers that identify them as T cells that have recently been stimulated through their antigen-specific receptor. These putatively disease-relevant T cells represent only a very minor fraction of tissue-infiltrating cells. Their preferential accumulation in the adventitia is most compatible with the model that they contact the relevant antigen primarily in this particular region of the artery. Their regulatory function appears to extend into the inner media and intima where pathological changes in
giant cell arteritis
are most pronounced.
...
PMID:Interferon-gamma-producing T cells in giant cell vasculitis represent a minority of tissue-infiltrating cells and are located distant from the site of pathology. 866 78