Immunophenotypic analysis of the aortic wall in Takayasu's arteritis: involvement of lymphocytes. dendritic cells and granulocytes in immunoinflammatory reactions
Sj. Inder et al., Immunophenotypic analysis of the aortic wall in Takayasu's arteritis: involvement of lymphocytes. dendritic cells and granulocytes in immunoinflammatory reactions, CARDIOV SUR, 8(2), 2000, pp. 141-148
The present study was undertaken to examine the cellular composition of the
aortic wall in Takayasu's arteritis and to investigate the association of
different cell types in the immunoinflammatory reactions of this disease, S
pecimens of aortic wall affected by Takayasu's arteritis were obtained from
10 patients (five male, five female), aged 32 to 68 years (mean 49.5 years
) at elective operation. The mean duration of disease was 6.5 years (range
2 months to 13 years). Specimens were embedded in paraffin and the sections
stained with antibodies to CD3 (to identify T cells), CD20 (B cells), S-10
0 (dendritic cells), CD15 (granulocytes), CD68 (macrophages), alpha-SMA (sm
ooth muscle cells) and von Willebrand factor (endothelial cells). Immunohis
tochemical examination demonstrated that all specimens showed histological
alteration with the replacement of the muscular and elastic layers of the m
edia and adventitia by dense fibrous tissue, and were characterized by vary
ing degrees of inflammatory cell infiltration. In five cases, inflammatory
nodules consisting of numerous T cells and B cells were observed in the adv
entitia, Within the inflammatory nodules, as well as around areas of neovas
cularization in the deep portion of the intima, lymphocytes were co-localiz
ed with dendritic cells, In addition, in the adventitia, the accumulation o
f a large number of granulocytes was observed, The present study demonstrat
es that immune inflammation is a typical feature of Takayasu's disease, and
that the interactions between dendritic cells and lymphocytes may be impor
tant in the control of the immune reactions in this vascular pathology. (C)
2000 Published by Elsevier Science Ltd. All rights reserved.