Epithelial dysplasia in Caroli ' s disease

نویسندگان

  • CONLETH FEIGHERY
  • DONALD WEIR
  • ALEX WHELAN
چکیده

SIR, -The comments of Drs Colombel, Janin, and Torpier are of interest. We agree that the immune processes which may contribute to the mucosal lesion of coeliac disease may be multifactorial. The eosinophil is a major component of the inflammatory infiltrate in coeliac disease, although this is frequently not emphasised in descriptions of the lesion. We have recently produced additional evidence that eosinophils and polymorphs are present in increased numbers in the coeliac mucosa: using monoclonal antibodies to Fc receptors (for the gamma chain ofIgG) types II and III, which are found on eosinophils and polymorphs, a marked increase in reactive cells was found. The evidence of Dr Colombel and colleagues that many of these eosinophils have degranulated and the associated finding of increased release of granule components points to mechanisms whereby eosinophils might mediate damage. The possibility that IgA, produced in large quantities in the damaged intestine, may be involved in eosinophil degranulation through interaction with IgA Fc receptors should also be considered. The finding that many coeliac patients react rapidly to gluten challenge (both symptomatically and histologically) is in keeping with more immediate mechanisms of damage also participating in the development of the lesion. Eosinophils are good candidates for such a mechanism. CONLETH FEIGHERY DONALD WEIR ALEX WHELAN StJaWles's Hospital, PO Box 580, Dublin 8, Ireland

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تاریخ انتشار 2006