2000 Volume 41 Issue 1 Pages 15-26
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 γδ T-cells as well as αβ T-cells and NK cells. The infiltrating γδ 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 γδ T-cells and αβ T-cells. T-cell receptor (TCR) αβ gene usage by the infiltrating cells was restricted, strongly suggesting that a specific antigen was targeted. TCR γδ 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 γδ T-cells in Takayasu arteritis because γδ 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. Jpn Heart J 2000; 41: 15-26)
