1993 Fiscal Year Final Research Report Summary
Function of KTH-1 antigen specific gamma delta +T cell clons derived from a patient with Behjets disease.
Project/Area Number |
03670334
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
内科学一般
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Research Institution | Saitama Medical Center, Saitama Medical School |
Principal Investigator |
KOIDE Jun Saitama Medical Center, Saitama Medical School 2nd Department of Medicine., 医学部, 講師 (70178193)
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Project Period (FY) |
1991 – 1993
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Keywords | Behcet's disease / Strepto.sanguis / KTH-1-Ag / gamma delta -TCR^+Tcell / TNF alpha / Cytotoxicity / Ca^<++>-influx |
Research Abstract |
IN the present study, we established also KTH-1-reactive three gamma delta +T cell clones and two CD4+ T cell clones more easily derived from peripheral blood in five patients with Behcet's disease. We show that these gamma delta clones express much more molecules of CD44 and VLA-1 than that of those CD4 clones, all of clones have proliferated vigorously in the response to KTH-1, but not rHSP(65KD), and the capacity of cytokine-production indicated the highest amounts of TNF alpha secreted by KTH-1-stimulated gamma delta clones, in contrast to moderate amounts of IL2 secreted by KTH-1-stimulated CD4 clones. Of interest was that the significant killing activity was shown by only gamma delta clones against NK-sensitive target cells, autologous and allogeneic EBV-transformed B cell lines, and this antivity was enhanced by a part of antibodies to CD44, or inhibited by tyrosine kinase-inhibitor(Herbimycin)in a different fashion. The most striking evidence was that there was quite difference of the changes in [Ca2+]i after KTH-1-stimulation of between gamma delta clones and CD4 clones by examination of single cell image analysis on ACAS.We suspected that these results indicated gamma delta +T cells, but not CD4+ T cell, have a central pathogenic role on the development of chronic inflammation after KTH-1-infection in Behcet's disease.
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