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Lymphocytic and collagenous colitis: an immunohistochemical study
J F Mosnier1, L Larvol, J Barge
1Service d'Anatomie et de Cytologie Pathologiques, Hôpital Beaujon, Clichy, France.
Insights
Immune abnormalities in lymphocytic colitis (LC) and collagenous colitis (CC) are similar, involving increased CD 8 intraepithelial lymphocytes (IELs) and abnormal HLA DR expression. These findings suggest a shared MHC-restricted immune mechanism distinct from celiac disease.
Area of Science:
- Gastroenterology
- Immunology
- Colorectal Pathology
Background:
- Lymphocytic colitis (LC) and collagenous colitis (CC) share increased intraepithelial lymphocytes (IELs).
- Similarities suggest a potential common underlying immune mechanism.
- Investigating IEL and lamina propria lymphocyte phenotypes is crucial.
Purpose of the Study:
- To determine the phenotype of IELs and lamina propria lymphocytes in LC and CC.
- To compare immune cell profiles between LC, CC, and controls.
- To elucidate potential shared pathogenic pathways.
Main Methods:
- Immunohistochemical analysis of colonic and ileal biopsies from LC, CC, and control groups.
- Utilized monoclonal antibodies targeting T-cells (CD4, CD8), HLA DR, and T-cell receptor (TcR) variants (alpha beta, gamma delta).
- Examined IELs and lamina propria lymphocytes across all bowel segments.
Main Results:
- Both LC and CC showed increased IEL counts, with a predominance of CD 8 IELs over CD 4 IELs.
- Most IELs expressed TcR alpha beta; TcR gamma delta-bearing cells were not elevated.
- CD 4+ helper T-cells were predominant in the lamina propria, and epithelial cells abnormally expressed HLA DR antigens.
Conclusions:
- Immune abnormalities in LC and CC are similar, pointing to a potential MHC-restricted immune mechanism.
- Evidence includes CD 4+ T-cell accumulation, CD 8 TcR alpha beta IEL-related epithelial damage, and abnormal HLA DR expression.
- The immune mechanisms in LC/CC likely differ from those in celiac disease.
Objectives:
An increase of intraepithelial lymphocytes (IEL) is commonly found in lymphocytic colitis (LC) and collagenous colitis (CC), and has also been observed in the colonic mucosa of some patients with celiac disease or celiac-like disease. Thus, a similar mechanism could play a role in these apparently different entities. The aim of this work was to determine the phenotype of IEL and of lamina propria lymphocytes 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 study 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 increased in mean numbers of IELs in both LC and 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 increased in CC or LC. CD 4+ helper T-cells predominated in the lamina propria. Epithelial cells of colonic mucosa abnormally expressed HLA DR antigens. There were no significant differences between findings in LC and CC.
Conclusion:
This study suggests that the immune abnormalities are similar in LC and CC and that a MHC-restricted immune mechanism could be involved in both diseases. Evidence for this includes: 1) the accumulation of CD 4+ T-cells within the lamina propria, 2) epithelial damage closely related to the increase of CD 8 TcR alpha beta IELs, and 3) abnormal class II MHC molecule expression on epithelial cells of colonic mucosa. Furthermore, the results suggest that the putative immune mechanisms underlying LC or CC are probably different from those that are incriminated in celiac disease.