Literature DB >> 10069909

Immunohistochemical analysis of arterial wall cellular infiltration in Buerger's disease (endarteritis obliterans).

M Kobayashi1, M Ito, A Nakagawa, N Nishikimi, Y Nimura.   

Abstract

PURPOSE: The diagnosis of Buerger's disease has depended on clinical symptoms and angiographic findings, whereas pathologic findings are considered to be of secondary importance. Arteries from patients with Buerger's tissue were analyzed histologically, including immunophenotyping of the infiltrating cells, to elucidate the nature of Buerger's disease as a vasculitis.
METHODS: Thirty-three specimens from nine patients, in whom Buerger's disease was diagnosed on the basis of our clinical and angiographic criteria between 1980 and 1995 at Nagoya University Hospital, were studied. Immunohistochemical studies were performed on paraffin-embedded tissue with a labeled streptoavidin-biotin method.
RESULTS: The general architecture of vessel walls was well preserved regardless of the stage of disease, and cell infiltration was observed mainly in the thrombus and the intima. Among infiltrating cells, CD3(+) T cells greatly outnumbered CD20(+) B cells. CD68(+) macrophages or S-100(+) dendritic cells were detected, especially in the intima during acute and subacute stages. All cases except one showed infiltration by the human leukocyte antigen-D region (HLA-DR) antigen-bearing macrophages and dendritic cells in the intima. Immunoglobulins G, A, and M (IgG, IgA, IgM) and complement factors 3d and 4c (C3d, C4c) were deposited along the internal elastic lamina.
CONCLUSION: Buerger's disease is strictly an endarteritis that is introduced by T-cell mediated cellular immunity and by B-cell mediated humoral immunity associated with activation of macrophages or dendritic cells in the intima.

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Year:  1999        PMID: 10069909     DOI: 10.1016/s0741-5214(99)70273-9

Source DB:  PubMed          Journal:  J Vasc Surg        ISSN: 0741-5214            Impact factor:   4.268


  16 in total

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8.  Possible involvement of Notch signaling in the pathogenesis of Buerger's disease.

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9.  Are There Any Objections against Our Hypothesis That Buerger Disease Is an Infectious Disease?

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10.  Activation of cytokines corroborate with development of inflammation and autoimmunity in thromboangiitis obliterans patients.

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