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Immunohistochemical analysis of mucosal gamma-interferon production in coeliac disease
A al-Dawoud1, I Nakshabendi, A Foulis
1Department of Pathology, Royal Infirmary, Glasgow.
Insights
Gamma-interferon plays a role in coeliac disease pathogenesis. Studies show reduced gamma-interferon expressing lymphocytes in coeliac patients, suggesting non-gamma-interferon cells drive inflammation.
Area of Science:
- Immunology
- Gastroenterology
- Cellular Biology
Background:
- The precise role of gamma-interferon in immune-mediated enteropathies like coeliac disease remains elusive.
- Understanding immune cell function is crucial for coeliac disease pathogenesis.
Purpose of the Study:
- To quantify gamma-interferon immunoreactive lymphocytes in coeliac disease jejunal biopsies.
- To compare these findings with normal controls and gluten-free diet treated patients.
Main Methods:
- Quantification of gamma-interferon expressing lymphocytes in jejunal biopsies.
- Immunohistochemical analysis of intraepithelial and lamina propria lymphocytes.
- Assessment of Class II Major Histocompatibility Complex expression on epithelial cells.
Main Results:
- Coeliac disease patients showed significantly lower percentages of gamma-interferon expressing intraepithelial (3.5%) and lamina propria (10.3%) lymphocytes compared to controls (13.5% and 47.2%, respectively).
- Treated coeliac patients had increased intraepithelial lymphocytes expressing gamma-interferon (10.3%).
- Epithelial cells in coeliac disease exhibited increased Class II Major Histocompatibility Complex expression, while intraepithelial lymphocytes were negative.
Conclusions:
- A substantial proportion of lymphocytes in the normal small intestine express gamma-interferon.
- The increase in mucosal lymphocytes in coeliac disease is primarily due to infiltration by lymphocytes lacking gamma-interferon expression.
- This suggests a distinct immune cell profile in active coeliac disease.
Abstract:
The role of gamma-interferon in the pathogenesis of enteropathies with an immunological basis such as coeliac disease, is unclear. Gamma-interferon immunoreactive lymphocytes were quantified in jejunal biopsies from patients with coeliac disease and from normal controls. In coeliac disease, there was an apparent decrease in the percentage of both intraepithelial (3.5% v 13.5%) and lamina propria (10.3% v 47.2%) lymphocytes expressing gamma-interferon compared with controls. In patients successfully treated with a gluten free diet, the percentage of gamma-interferon immunoreactive intra-epithelial lymphocytes was 10.3%. Intraepithelial lymphocytes were immunonegative for class II major histocompatibility complex, while epithelial cells showed increased expression of this product in coeliac disease. The results show that a relatively large proportion of lymphocytes in normal small bowel express gamma-interferon. They also indicate that in coeliac disease the major increase in the numbers of mucosal lymphocytes is the result of infiltration by lymphocytes not expressing gamma-interferon.
