Abstract
Takayasu's arteritis is an inflammatory disease of the arteries that involves large vessels. The inflammatory lesions in Takayasu's arteritis originate in the vasa vasorum and are followed by cellular infiltration, mainly composed of T cells (γδ lymphocytes, cytotoxic T lymphocytes, T helper cells), but also of natural killer cells, dendritic cells, monocytes and granulocytes, invading the outer layer of the media and/or its neighbouring adventitia. At this stage, positive production of inflammatory cytokines and/or adhesion molecules around these areas is remarkable. According to data available - in Takayasu's arteritis-interleukin-6, interleukin-1 and RANTES are released in large amounts by infiltrating inflammatory cells within damaged tissue, as well as by circulating inflammatory cells, and very likely help maintain the aberrant immune activation, by promoting endothelial cells activation and by inducing lymphocyte infiltration. Although the nature of the antigen that triggers the auto-immune process is still unknown, the infiltrating T lymphocytes may recognize one or a few self-antigens processed and presented in association with HLA. A considerable percentage of patients with Takayasu's arteritis have immune complexes in sera; moreover, on peripheral blood lymphocyte, Fc receptors and antibodies reactive against human endothelial cells (AECA) have been detected. This observation raised the possibility that AECA might have a role in endothelial cell activation and expression of adhesion molecules, which will facilitate leukocyte traffic.
| Original language | English |
|---|---|
| Pages (from-to) | 506-513 |
| Number of pages | 8 |
| Journal | Journal of Nephrology |
| Volume | 14 |
| Issue number | 6 |
| Publication status | Published - 2001 |
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Keywords
- γδ lymphocytes
- Anti-endothelial cell antibodies
- Chemokines
- Cytokines
- Takayasu's arteritis
ASJC Scopus subject areas
- Nephrology
Cite this
Pathogenesis of Takayasu's arteritis. / Noris, Marina.
In: Journal of Nephrology, Vol. 14, No. 6, 2001, p. 506-513.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Pathogenesis of Takayasu's arteritis
AU - Noris, Marina
PY - 2001
Y1 - 2001
N2 - Takayasu's arteritis is an inflammatory disease of the arteries that involves large vessels. The inflammatory lesions in Takayasu's arteritis originate in the vasa vasorum and are followed by cellular infiltration, mainly composed of T cells (γδ lymphocytes, cytotoxic T lymphocytes, T helper cells), but also of natural killer cells, dendritic cells, monocytes and granulocytes, invading the outer layer of the media and/or its neighbouring adventitia. At this stage, positive production of inflammatory cytokines and/or adhesion molecules around these areas is remarkable. According to data available - in Takayasu's arteritis-interleukin-6, interleukin-1 and RANTES are released in large amounts by infiltrating inflammatory cells within damaged tissue, as well as by circulating inflammatory cells, and very likely help maintain the aberrant immune activation, by promoting endothelial cells activation and by inducing lymphocyte infiltration. Although the nature of the antigen that triggers the auto-immune process is still unknown, the infiltrating T lymphocytes may recognize one or a few self-antigens processed and presented in association with HLA. A considerable percentage of patients with Takayasu's arteritis have immune complexes in sera; moreover, on peripheral blood lymphocyte, Fc receptors and antibodies reactive against human endothelial cells (AECA) have been detected. This observation raised the possibility that AECA might have a role in endothelial cell activation and expression of adhesion molecules, which will facilitate leukocyte traffic.
AB - Takayasu's arteritis is an inflammatory disease of the arteries that involves large vessels. The inflammatory lesions in Takayasu's arteritis originate in the vasa vasorum and are followed by cellular infiltration, mainly composed of T cells (γδ lymphocytes, cytotoxic T lymphocytes, T helper cells), but also of natural killer cells, dendritic cells, monocytes and granulocytes, invading the outer layer of the media and/or its neighbouring adventitia. At this stage, positive production of inflammatory cytokines and/or adhesion molecules around these areas is remarkable. According to data available - in Takayasu's arteritis-interleukin-6, interleukin-1 and RANTES are released in large amounts by infiltrating inflammatory cells within damaged tissue, as well as by circulating inflammatory cells, and very likely help maintain the aberrant immune activation, by promoting endothelial cells activation and by inducing lymphocyte infiltration. Although the nature of the antigen that triggers the auto-immune process is still unknown, the infiltrating T lymphocytes may recognize one or a few self-antigens processed and presented in association with HLA. A considerable percentage of patients with Takayasu's arteritis have immune complexes in sera; moreover, on peripheral blood lymphocyte, Fc receptors and antibodies reactive against human endothelial cells (AECA) have been detected. This observation raised the possibility that AECA might have a role in endothelial cell activation and expression of adhesion molecules, which will facilitate leukocyte traffic.
KW - γδ lymphocytes
KW - Anti-endothelial cell antibodies
KW - Chemokines
KW - Cytokines
KW - Takayasu's arteritis
UR - http://www.scopus.com/inward/record.url?scp=0035714982&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035714982&partnerID=8YFLogxK
M3 - Article
C2 - 11783607
AN - SCOPUS:0035714982
VL - 14
SP - 506
EP - 513
JO - Journal of Nephrology
JF - Journal of Nephrology
SN - 1121-8428
IS - 6
ER -