1998 Fiscal Year Final Research Report Summary
Role of alphaEbeta7 on tissue destruction of autoimmune diseases
| Project/Area Number |
09670491
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内科学一般
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| Research Institution | Saitama Medical School |
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Principal Investigator |
TAKEUCHI Tsutomu Saitama Medical School Professor, 医学部, 教授 (50179610)
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| Co-Investigator(Kenkyū-buntansha) |
AMANO Kouichi Saitama Medical School Assist Prof, 医学部, 講師 (00175928)
TSUZAKA Kensei Saitama Medical School Instructor, 医学部, 助手 (00245490)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Integrins / autoimmunity / SLE / epithelial cells / E-cadherin / adhesion / apoptosis |
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| Research Abstract |
To characterize the activated PBL and the role on pathogenesis in SLE, we have developed a series of monoclonal antibodies directed against the surface structures on the SLE PBL.We focused on the one monoclonal antibody designated SM-17, which reacted to the activation antigen on CD8+T cells. immunoprecipitation analysis clearly showed that the antigen recognized by SM-17 was alpha^Ebeta_7 (CD 103), which was first identified the surface antigen on the intra-epithelial lymphocytes. The expression of alpha^Ebeta_7 (CD 103) was examined in the a variety of autoimmtme and hematological patients with or without stimulation of PHA.We found that the expression of alpha^Ebeta_7 (CD 103) was significantly elevated in patients with SLE after stimulation with PHA, and one patient with hairy cell leukemia in the absence of stimulation. The enhanced expression was not only observed in CD8+ T cells, but also in CD4+ T cells from SLE patients. Th enhanced expression of CD 103 is significantly correlated with the presence of oral ulcers or serositis, suggesting that it may involve in tissue injury in these sites. Adhesion experiments against the HSG epithelial cell lines showed that the T cells with enhanced expression of CD 103 strongly adhered onto HSG, which was partially blocked by anti-alpha^Ebeta_7 antibody. These results suggest a role of this novel inte grin on the tissue injury, particularly epithelial cells, which are expressing E-cadherin, a higand for CD 103.
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