Autoimmunity in ulcerative colitis: humoral and cellular immune response bytropomyosin in ulcerative colitis

AIM Autoimmunity has been emphasized in the pathogenesis of ulcerative colitis (UC). We reported thattropomyosin (TM) or TM related protein is a putative autoantigen in UC. In human fibroblast, at least 8isoforms of TM have been identified with molecular weight range from 30kD to 40kD, depending upo...

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Veröffentlicht in:世界胃肠病学杂志(英文版) 2000, Vol.6 (3), p.9
Hauptverfasser: Xin Geng, Masato Taniguchi, Hui Hui Dai, JJ-C Lin, Jim Lin, Kiron Moy Das
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Sprache:eng
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Zusammenfassung:AIM Autoimmunity has been emphasized in the pathogenesis of ulcerative colitis (UC). We reported thattropomyosin (TM) or TM related protein is a putative autoantigen in UC. In human fibroblast, at least 8isoforms of TM have been identified with molecular weight range from 30kD to 40kD, depending upon theisoforms, and human TM isoforms (hTM5) has been found the main isoform in human intestinal epithelialcells. In this study, hTM5 was used as a putative auto-antigen for the humoral and T cell immune responses inpatients with UC, Crohn's disease (CD) and healthy subjects (HS) as controls.METHODS Anti-bTM antibody was examined by enzyme-linked immunosorbent assay using human sera(UC 59, CD 28, HS 26) against hTM isoforms. The IFN-γ production by peripheral blood T cells followingstimulation by recombinant hTM5 was analyzed by ELISPOT assay.RESULTS Anti-hTM5 antibody (IgG1) was detected in 15/59 (25.4%) patients with UC, 3/28 (10.γ%)with CD, and 3/26 (11.5%) of HS. The OD value in UC was significantly higher than in CD and HS groups(P < 0.05; P < 0.01 respectively). Western blot analysis demonstrated immunoreactivity against hTM5 inseveral UC sera. ELISPOT assay demonstrated that IFN-γ production is significantly higher in UC (7/18),39.0%), compared with CD (0/8, 0%) and HS (0/7, 0%), (P<0.05).CONCLUSION A significantly higher immune response to hTM5 was present in UC compared to CD andHS. Further studies of the hTM5/peptides may provide immuno-biochemical mechanism of autoimmuneprocess in UC.
ISSN:1007-9327