The Th1/Th2 immune-type response of the recurrent aphthous ulceration analyzed by cDNA microarray
Background: The reduced ability to activate oral tolerance plays a role in the pathogenesis of some gastrointestinal inflammatory diseases. This activation may reflect a preferential reduction of a T‐helper (Th)2‐ or Th3‐type response. In recurrent aphthous ulceration (RAU), genetic and environment...
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Published in | Journal of oral pathology & medicine Vol. 33; no. 3; pp. 140 - 146 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Munksgaard International Publishers
01.03.2004
Blackwell |
Subjects | |
Online Access | Get full text |
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Summary: | Background: The reduced ability to activate oral tolerance plays a role in the pathogenesis of some gastrointestinal inflammatory diseases. This activation may reflect a preferential reduction of a T‐helper (Th)2‐ or Th3‐type response. In recurrent aphthous ulceration (RAU), genetic and environmental factors may contribute to low tolerance, permitting a cytotoxic reaction against the oral epithelium. The cytokine profile has not permitted the definition of RAU as resulting from enhanced Th1 or Th2 responses. A cDNA microarray study would allow the identification of differentially expressed genes and provide a basis for classification of the immune response.
Methods: The cDNA from 29 samples of aphthae and from 11 samples of normal mucosa from aphthae‐free volunteers were hybridized on microarray membranes with 1176 genes.
Results: Forty‐one differentially expressed genes were identified, and a higher expression level of the Th1 gene cluster in RAU was found.
Conclusions: Microarrays permitted us definition of the gene expression profile of the lesion and identify an increased Th1 activity in RAU lesions. |
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Bibliography: | ark:/67375/WNG-DJ3PMZ5X-5 istex:0FD6D02ABCD653B8F697E4F0DB7345CB8E0E5DCA ArticleID:JOP089 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0904-2512 1600-0714 |
DOI: | 10.1111/j.0904-2512.2004.00089.x |