Takayasu's arteritis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* The pathogenesis of Takayasu's arteritis is poorly understood.<ref name="pmid10737351">{{cite journal |vauthors=Inder SJ, Bobryshev YV, Cherian SM, Wang AY, Lord RS, Masuda K, Yutani C |title=Immunophenotypic analysis of the aortic wall in Takayasu's arteritis: involvement of lymphocytes, dendritic cells and granulocytes in immuno-inflammatory reactions |journal=Cardiovasc Surg |volume=8 |issue=2 |pages=141–8 |date=March 2000 |pmid=10737351 |doi= |url=}}</ref> | * The pathogenesis of Takayasu's arteritis is poorly understood.<ref name="pmid10737351">{{cite journal |vauthors=Inder SJ, Bobryshev YV, Cherian SM, Wang AY, Lord RS, Masuda K, Yutani C |title=Immunophenotypic analysis of the aortic wall in Takayasu's arteritis: involvement of lymphocytes, dendritic cells and granulocytes in immuno-inflammatory reactions |journal=Cardiovasc Surg |volume=8 |issue=2 |pages=141–8 |date=March 2000 |pmid=10737351 |doi= |url=}}</ref> | ||
* Takayasu's arteritis characterized by segmental and patchy [[Granuloma|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 [[Aneurysm|aneurysms]]. | |||
* There is also irregular fibrosis of the blood vessels due to chronic vasculitis, leading to sometimes massive intimal fibrosis. | |||
* Three factors have been suggested that have associated with disease susceptibility, development and progression: | * Three factors have been suggested that have associated with disease susceptibility, development and progression: | ||
** Relationship to [[tuberculosis]] (TB) | ** Relationship to [[tuberculosis]] (TB) | ||
| Line 19: | Line 23: | ||
'''Genetic influences''' | '''Genetic influences''' | ||
Geographic distribution of Takayasu arteritis, with high prevalence in Japan and Korea, suggests that genetic factors are probably play a role in the pathogenesis of Takayasu arteritis. | |||
* Takayasu arteritis has been associated with different [[Human leukocyte antigen|human leucocyte antigen]] ([[Human leukocyte 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> | |||
'''Immunologic mechanisms''' | '''Immunologic mechanisms''' | ||
* Immunohistopathologic examination has shown that the infiltrating cells in aortic tissue mainly consist of killer cells, especially gamma delta T lymphocytes | * 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 | * These cells may cause vascular injury by releasing large amounts of the cytolytic compound perforin | ||
* 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> | ||
* 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. | * 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: | * The most important conditions associated with Takayasu's arteritis include: | ||
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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]
- 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.
- There is also irregular fibrosis of the blood vessels due to chronic vasculitis, leading to sometimes massive intimal fibrosis.
- 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
Geographic distribution of Takayasu arteritis, with high prevalence in Japan and Korea, suggests that genetic factors are probably play a role in the pathogenesis of Takayasu arteritis.
- 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.[3]
Immunologic mechanisms
- 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
- 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.[4]
- 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.
- ↑ 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.
- ↑ 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.