LYMPHOCYTIC AND COLLAGENOUS COLITIS - AN IMMUNOHISTOCHEMICAL STUDY

Citation
Jf. Mosnier et al., LYMPHOCYTIC AND COLLAGENOUS COLITIS - AN IMMUNOHISTOCHEMICAL STUDY, The American journal of gastroenterology, 91(4), 1996, pp. 709-713
Citations number
34
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00029270
Volume
91
Issue
4
Year of publication
1996
Pages
709 - 713
Database
ISI
SICI code
0002-9270(1996)91:4<709:LACC-A>2.0.ZU;2-0
Abstract
Objectives: An increase of intraepithelial lymphocytes (IEL) is common ly found in lymphocytic colitis (LC) and collagenous colitis (CC), and has also been observed in the colonic mucosa of some patients with ce liac disease or celiac-like disease. Thus, a similar mechanism could p lay a role in these apparently different entities. The aim of this wor k was to determine the phenotype of IEL and of lamina propria lymphocy tes in the setting of LC and CC. Methods: Biopsies were taken from all segments of the large bowel and from the ileon of eight patients with CC, four patients with LC, and 10 controls. An immunohistochemical st udy using monoclonal antibodies directed against IEL, T-cells, helper T-cells, suppressor/cytotoxic T-cells, HLA DR antigens, T-cell-bearing T-cell receptor (TcR) alpha beta, and TcR gamma delta was carried out . Results: There was an increase in mean numbers of IELs in both LC an d CC, with significantly more CD 8 IELs than CD 4 IELs. Most IELs were bearing TcR alpha beta; TcR gamma delta-bearing cells were not increa sed in CC or LC. CD 4+ helper T-cells predominated in the lamina propr ia. Epithelial cells of colonic mucosa abnormally expressed HLA DR ant igens. There were no significant differences between findings in LC an d CC. Conclusion: This study suggests that the immune abnormalities ar e similar in LC and CC and that a MHC-restricted immune mechanism coul d be involved in both diseases; Evidence for this includes: 1) the acc umulation of CD 4+ T-cells within the lamina propria, 2) epithelial da mage closely related to the increase of CD 8 TcR alpha beta IELs, and 3) abnormal class II MHC molecule expression on epithelial cells of co lonic mucosa. Furthermore, the results suggest that the putative immun e mechanisms underlying LC or CC are probably different from those tha t are incriminated in celiac disease.