PMID- 10807525
OWN - NLM
STAT- MEDLINE
DCOM- 20000523
LR  - 20190826
IS  - 0021-4868 (Print)
IS  - 0021-4868 (Linking)
VI  - 41
IP  - 1
DP  - 2000 Jan
TI  - Takayasu arteritis: insights into immunopathology.
PG  - 15-26
AB  - Takayasu arteritis is an acute and sometimes chronic form of vasculitis involving 
      the aorta, its main branches and pulmonary arteries. Although its etiology is 
      still unknown, immunopathologic analyses revealed that the infiltrating cells 
      mainly consisted of gammadelta T-cells as well as alphabeta T-cells and NK cells. 
      The infiltrating gammadelta T-cells, cytotoxic T-lymphocytes (CTLs), and natural 
      killer (NK) cells directly injured the vascular cells by releasing a cytolytic 
      factor, perforin. Expression of heat-shock protein (HSP)-65 as well as human 
      leukocyte antigen (HLA) class I and II was enhanced in Takayasu arteritis 
      lesions, supporting the pathogenic role of gammadelta T-cells and alphabeta 
      T-cells. T-cell receptor (TCR) alphabeta gene usage by the infiltrating cells was 
      restricted, strongly suggesting that a specific antigen was targeted. TCR 
      gammadelta gene usage by the infiltrating cells was also restricted. Furthermore, 
      it has been reported that a strong association with a specific haplotype of major 
      histocompatibility complex (MHC) class I chain-related (MIC), MICA gene with 
      Takayasu arteritis, suggesting that the HLA-linked gene susceptible to the 
      disease is mapped near the MICA gene. This also supports a pathogenic role of 
      gammadelta T-cells in Takayasu arteritis because gammadelta T-cells were shown to 
      recognize MICA molecule, which can be stress-induced. These findings suggest that 
      unknown stress, such as infection, may trigger the autoimmune process of 
      inflammation involved in Takayasu arteritis.
FAU - Seko, Y
AU  - Seko Y
AD  - Department of Cardiovascular Medicine, Graduate School of Medicine, University of 
      Tokyo, Japan.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Japan
TA  - Jpn Heart J
JT  - Japanese heart journal
JID - 0401175
RN  - 0 (HLA Antigens)
SB  - IM
MH  - Aorta/pathology
MH  - Genetic Predisposition to Disease
MH  - HLA Antigens/analysis
MH  - Humans
MH  - T-Lymphocytes/immunology
MH  - Takayasu Arteritis/genetics/*immunology/pathology
RF  - 61
EDAT- 2000/05/12 09:00
MHDA- 2000/06/08 09:00
CRDT- 2000/05/12 09:00
PHST- 2000/05/12 09:00 [pubmed]
PHST- 2000/06/08 09:00 [medline]
PHST- 2000/05/12 09:00 [entrez]
AID - 10.1536/jhj.41.15 [doi]
PST - ppublish
SO  - Jpn Heart J. 2000 Jan;41(1):15-26. doi: 10.1536/jhj.41.15.