Takayasu's arteritis pathophysiology: Difference between revisions
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'''Relationship to tuberculosis (TB)''' | '''Relationship to tuberculosis (TB)''' | ||
[[Granulomatous]] inflammation with the Langhans-type of [[giant cells]] in many cases of Takayasu arteritis and the intermittent coexistence of Takayasu arteritis with pulmonary and extrapulmonary tuberculosis, support this idea. However,the absence of [[mycobacterial]] organisms in arteritic lesions and the lack of response to anti-tuberculus therapy suggest that perhaps [[hypersensitivity]] to the tuberculus organism may play a role in the pathogenesis of Takayasu arteritis.<ref name="pmid12655" /> | [[Granulomatous]] inflammation with the Langhans-type of [[giant cells]] in many cases of Takayasu arteritis and the intermittent coexistence of Takayasu arteritis with pulmonary and extrapulmonary tuberculosis, support this idea. However,the absence of [[mycobacterial]] organisms in arteritic lesions and the lack of response to anti-tuberculus therapy suggest that perhaps [[hypersensitivity]] to the tuberculus organism may play a role in the pathogenesis of Takayasu arteritis.<ref name="pmid12655">{{cite journal |vauthors=Lupi-Herrera E, Sánchez-Torres G, Marcushamer J, Mispireta J, Horwitz S, Vela JE |title=Takayasu's arteritis. Clinical study of 107 cases |journal=Am. Heart J. |volume=93 |issue=1 |pages=94–103 |date=January 1977 |pmid=12655 |doi= |url=}}</ref> | ||
'''Genetic influences''' | '''Genetic influences''' | ||
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* There is also irregular fibrosis of the blood vessels due to chronic vasculitis, leading to sometimes massive intimal fibrosis. | * There is also irregular fibrosis of the blood vessels due to chronic vasculitis, leading to sometimes massive intimal fibrosis. | ||
* Seko ''et al'' have reported that γδT cells, αβT cells (CD4 and CD8), and natural killer cells play an important role in the vascular injury.<ref name="pmid10980341">{{cite journal |vauthors=Seko Y, Takahashi N, Tada Y, Yagita H, Okumura K, Nagai R |title=Restricted usage of T-cell receptor Vgamma-Vdelta genes and expression of costimulatory molecules in Takayasu's arteritis |journal=Int. J. Cardiol. |volume=75 Suppl 1 |issue= |pages=S77–83; discussion S85–7 |date=August 2000 |pmid=10980341 |doi= |url=}}</ref> | * Seko ''et al'' have reported that γδT cells, αβT cells (CD4 and CD8), and natural killer cells play an important role in the vascular injury.<ref name="pmid10980341">{{cite journal |vauthors=Seko Y, Takahashi N, Tada Y, Yagita H, Okumura K, Nagai R |title=Restricted usage of T-cell receptor Vgamma-Vdelta genes and expression of costimulatory molecules in Takayasu's arteritis |journal=Int. J. Cardiol. |volume=75 Suppl 1 |issue= |pages=S77–83; discussion S85–7 |date=August 2000 |pmid=10980341 |doi= |url=}}</ref> | ||
* Takayasu arteritis has been associated with different human leucocyte antigen (HLA) alleles in different populations. | * Takayasu arteritis has been associated with different human leucocyte antigen (HLA) alleles in different populations. | ||
* in Japan and Korea there is a clear association with the extended haplotype: HLA B*52, DRB1*1502, DRB5*0102, DQA1*0103, DQB1*0601, DPA1*02-DPB1*0901.<ref name="pmid10980348">{{cite journal |vauthors=Salazar M, Varela A, Ramirez LA, Uribe O, Vasquez G, Egea E, Yunis EJ, Iglesias-Gamarra A |title=Association of HLA-DRB1*1602 and DRB1*1001 with Takayasu arteritis in Colombian mestizos as markers of Amerindian ancestry |journal=Int. J. Cardiol. |volume=75 Suppl 1 |issue= |pages=S113–6 |date=August 2000 |pmid=10980348 |doi= |url=}}</ref> | * in Japan and Korea there is a clear association with the extended haplotype: HLA B*52, DRB1*1502, DRB5*0102, DQA1*0103, DQB1*0601, DPA1*02-DPB1*0901.<ref name="pmid10980348">{{cite journal |vauthors=Salazar M, Varela A, Ramirez LA, Uribe O, Vasquez G, Egea E, Yunis EJ, Iglesias-Gamarra A |title=Association of HLA-DRB1*1602 and DRB1*1001 with Takayasu arteritis in Colombian mestizos as markers of Amerindian ancestry |journal=Int. J. Cardiol. |volume=75 Suppl 1 |issue= |pages=S113–6 |date=August 2000 |pmid=10980348 |doi= |url=}}</ref> | ||
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** Inflammatory bowel disease (IBD) | ** Inflammatory bowel disease (IBD) | ||
** Behçet's syndrome (BS) | ** Behçet's syndrome (BS) | ||
==References== | ==References== |
Revision as of 16:01, 5 April 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]
Overview
Pathophysiology
- The pathogenesis of Takayasu's arteritis is poorly understood.[1]
- Three factors have been suggested that have associated with disease susceptibility, development and progression:
- Relationship to tuberculosis (TB)
- Genetic influences
- Immunologic mechanisms
Relationship to tuberculosis (TB)
Granulomatous inflammation with the Langhans-type of giant cells in many cases of Takayasu arteritis and the intermittent coexistence of Takayasu arteritis with pulmonary and extrapulmonary tuberculosis, support this idea. However,the absence of mycobacterial organisms in arteritic lesions and the lack of response to anti-tuberculus therapy suggest that perhaps hypersensitivity to the tuberculus organism may play a role in the pathogenesis of Takayasu arteritis.[2]
Genetic influences
Immunologic mechanisms
- Takayasu's arteritis characterized by segmental and patchy granulomatous inflammation of the aorta and its major derivative branches.
- Cell-mediated mechanisms are thought to be of primary importance and may be similar to those in giant cell arteritis.
- This inflammation leads to arterial stenosis, thrombosis, and aneurysms.
- Immunohistopathologic examination has shown that the infiltrating cells in aortic tissue mainly consist of killer cells, especially gamma delta T lymphocytes
- These cells may cause vascular injury by releasing large amounts of the cytolytic compound perforin
- There is also irregular fibrosis of the blood vessels due to chronic vasculitis, leading to sometimes massive intimal fibrosis.
- Seko et al have reported that γδT cells, αβT cells (CD4 and CD8), and natural killer cells play an important role in the vascular injury.[3]
- Takayasu arteritis has been associated with different human leucocyte antigen (HLA) alleles in different populations.
- in Japan and Korea there is a clear association with the extended haplotype: HLA B*52, DRB1*1502, DRB5*0102, DQA1*0103, DQB1*0601, DPA1*02-DPB1*0901.[4]
- The genetic contribution to the pathogenesis of Takayasu's arteritis is supported by the genetic association with HLA-B∗52.
- no specific autoantigens have yet been identified and for any adaptive immune response to occur, whether against exogenous or endogenous antigen, presentation of antigen to T cells in the context of the major histocompatibility complex is central.
- The most important conditions associated with Takayasu's arteritis include:
- Ankylosing spondylitis(AS)
- Inflammatory bowel disease (IBD)
- Behçet's syndrome (BS)
References
- ↑ Inder SJ, Bobryshev YV, Cherian SM, Wang AY, Lord RS, Masuda K, Yutani C (March 2000). "Immunophenotypic analysis of the aortic wall in Takayasu's arteritis: involvement of lymphocytes, dendritic cells and granulocytes in immuno-inflammatory reactions". Cardiovasc Surg. 8 (2): 141–8. PMID 10737351.
- ↑ Lupi-Herrera E, Sánchez-Torres G, Marcushamer J, Mispireta J, Horwitz S, Vela JE (January 1977). "Takayasu's arteritis. Clinical study of 107 cases". Am. Heart J. 93 (1): 94–103. PMID 12655.
- ↑ Seko Y, Takahashi N, Tada Y, Yagita H, Okumura K, Nagai R (August 2000). "Restricted usage of T-cell receptor Vgamma-Vdelta genes and expression of costimulatory molecules in Takayasu's arteritis". Int. J. Cardiol. 75 Suppl 1: S77–83, discussion S85–7. PMID 10980341.
- ↑ Salazar M, Varela A, Ramirez LA, Uribe O, Vasquez G, Egea E, Yunis EJ, Iglesias-Gamarra A (August 2000). "Association of HLA-DRB1*1602 and DRB1*1001 with Takayasu arteritis in Colombian mestizos as markers of Amerindian ancestry". Int. J. Cardiol. 75 Suppl 1: S113–6. PMID 10980348.