1995 Fiscal Year Final Research Report Summary
Investigation of cause of Kawasaki disease, molecular infecto-immunolgical analysis
| Project/Area Number |
06454310
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | Kurume University |
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Principal Investigator |
KATO Hirohisa Kurume University, Medicine, Professor, 医学部, 教授 (30080724)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAGUCHI Minako Kurume University, Medicine, Assisant Professor, 医学部, 助手 (50258422)
NISHIYORI Atsushi Kurume University, Medicine, Assistant Professor, 医学部, 助手 (30218226)
SATO Noboru Kurume University, Medicine, Assistant Professor, 医学部, 助手 (50205952)
SAGAWA Kimitaka Kurume University, Medicine, Professor, 医学部, 教授 (20140650)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Kawasaki disease / T cell receptor / super antigen |
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| Research Abstract |
The etiology of KD is unknown. Some reports indicated that KD is associated with the selective expansion of Vbeta2^+ and Vbeta8.1^+T cells in peripheral blood lymphocytes (PBL). To understand better the ethiology of KD,we investigated T cell receptor (TCR) Vbeta^<2+> and Vbeta8.1^+ expansion on the T cell of freshly isolated PBL and T cell clones (TCC). Blood samples were obtained from patients with acute (n=20) and convalescent (n=20) KD,age matched children with non-infectious disease (n=18), and healthy adults (n=20). Among these four groups, there were no significant differences in the percentages of their Vbeta^<2+> and Vbeta8.1^+T cells. The same was true for the CD4^+ or CD8^+ T cell subsets. One hundred and five TCC established from the affected skin, lymphnode or PBL of six patients with KD were also negative for either Vbeta2 or Vbeta8.1 TCR.Sixty-eight of 105 TCC produced detectable levels of TNF-alpha, in the absence of any stimuli. In contrast, only 11 or 7 produced detectable levels of IL-2 or IL-6, respectively. Stimulation with phytohaemagglutinin and phorbol myristate induced most TCC to produce higher amounts of TNF-alpha, IL-2 and IL-6. These results suggest that CD4^+ T helper cells expressing TCR-beta other than Vbeta2 or Vbeta8.1 receptor, primarily through TNF-alpha production, are involved in the immunopathology of KD.In other reports that KD is associated with the selective expansion of Vbeta2 and Vbeta8.1, in vitro activated PBL were used. Therfore, their method may allow possibly allow in vitro modification of TCR usage.
Fouthermore we measured TSST-1 concentrations and anti-TSST-1 antibody in serum from KD patients in both the acute and the convalescent phase. TSST-1 was reported as a possible cause of KD recently. Bur we failed to find any evidence that KD is caused by TSST-1.
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