| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
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| Research Abstract |
It is reported that a part of lamina propria lymphocytes (LPL) were expanded oligoclonally in patients with Crohn's disease. Furthermore, foreign antigenistic stimuli are reported to be closely related to the pathogenesis of Crohn's disease. In present study, we analyzed clonality of expanded lamina propria lymphocytes to elusidate whether they are persistently stimurated with antigens related to the disease. [Methods] Biopsy specimens during endoscopy were process to yield CD4^+ LPL by modified method of Bull and Bookman, and the magnetic beads labelled antibody method. Clonality of T cell receptor (TCR) Vbeta subsetswere analyzed by reverse transcriptase-polymerase. Chain reaction (RT-PCR) and single strand conformational polymorphism of CDR3 region of TCR Vbeta Clonality of periperal blood lymphocytes were compared to see mucosal immune activation. [Result] CD4^+LPL from all 12 patients with patients Crohn's disease showed oligoclonal expansion. Expanded Vbeta types were differed in each patient, however, most prominent Vbeta common to the patients group were Vbeta 2,5.1,5.2,13.1,19. There were no oligoclonality observed in CD4^+ LPL from patients with 5 cases with ulcertive colitis, 1radiation colitis or 5 control subjects. Peripheral blood lymphocytes from diseased and control subjects showed no oligoclonality. Interestingly, in 2 patients with Crohn's disease who have skipped lesions, same clone was persistently observed from different part of the invol ved intestine but not from uninvolved lesion. Common Vbeta subtype was Vbeta 5.1 in one patient and Vbeta 5.2 in the other.
[Conclusion]These results suggest the existence of conventional type antigenistic stimuli which may be presented by CD4-class II MHC in patients with Crohn's disease, and those specific antigens may play an impotant role in the pathogenesis of Crohn's disease.
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