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T cell receptor vß gene expression in inflammatory bowel disease lamina propria lymphocytes: evidence for altered vß gene usage.
Duchmann, R; Strober, W; Alling, D W; Fiocchi, C; James, S P.
  • Duchmann R; Mucosal Immunity Section, Laboratory of Clinical Investigation, and *Office of the Director of Intramural Research, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland; †Department of Gastroenterology and Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio; and ‡Division of Gastroenterology, Department of Medicine, University of Maryland at Baltimore, Baltimore, Maryland, U.S.A.
Inflamm Bowel Dis ; 1(3): 184-92, 1995.
Article en En | MEDLINE | ID: mdl-23282388
: In this study the TCR-Vß repertoire expressed in T cells of lamina propria mononuclear cells (LPMC) and peripheral blood mononuclear cells (PBMC) was examined using a reverse transcription-PCR (RT-PCR) technique for TCR-Vß mRNA. Using a qualitative RT-PCR method, LPMC of patients with IBD and control individuals were shown to contain mRNA for each of 20 TCR-Vß families, indicating that IBD is not associated with a major deletion or expansion of any TCR-Vß family. Subsequently, using a quantitative method for four frequently expressed TCR-Vß families, it was shown that the pattern of TCR-Vß expression was different in PBMC and LPMC of both IBD patients and control individuals. In addition, it was shown that the LPMC/PBMC ratio of mean mRNA values for TCR-Vß2, but not for TCR-Vß6, 7, and 14 was lower in IBD patients than control individuals. These results show that the TCR-Vß repertoire in PBMC and LPMC is different both in IBD patients and control individuals. In addition, they show that the TCR-Vß repertoire is altered in IBD, possibly due to an immune response to disease specific antigens, superantigens or neoantigens.
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Banco de datos: MEDLINE Tipo de estudio: Qualitative_research Idioma: En Año: 1995 Tipo del documento: Article
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Banco de datos: MEDLINE Tipo de estudio: Qualitative_research Idioma: En Año: 1995 Tipo del documento: Article