TIA1 and Mast Cell Tryptase in Food Allergy of Children: Increase of Intraepithelial Lymphocytes Expressing TIA1 Associates With Allergy

Author:

Augustin Merja1,Karttunen Tuomo J.1,Kokkonen Jorma2

Affiliation:

1. Departments of Pathology University of Oulu Oulu Finland

2. Department of Pediatrics University of Oulu Oulu Finland

Abstract

ABSTRACTBackgroundVariability of symptoms and signs make the diagnosis of children's food allergy (FA) difficult. In addition, mechanisms and antigens involved vary with age. In young infants, cow's milk protein allergy is associated with an increase of cytotoxic intraepithelial lymphocytes (IELs) expressing T‐cell–restricted intracellular antigen (TIA1). In the current study, the significance of TIA1 in FA in older children of mainly preschool and school age was analyzed and the findings correlated the with a detailed clinical, endoscopic, and histopathologic analysis.MethodsThe subjects of this study were 66 children (mean age, 7.9 years; range, 1–15), including 27 with untreated and 15 with treated FA, and 24 control subjects. The morphology of duodenal and antral biopsy specimens was evaluated, and the proportion of TIA1‐positive IELs was counted from immunostained sections. Quantification of mast cells with immunostaining for mast cell tryptase (MCT) was completed, with the estimation of diffuse extracellular staining considered to indicate degranulation.ResultsPatients with untreated FA showed an increase in the total number of TIA1‐positive cells and IELs and of the TIA1/IEL ratio. The number of mast cells in duodenal mucosa was decreased in children with FA, but no association with degranulation was observed. Endoscopic abnormalities were common in FA, but conventional histopathology showed no informative differences.ConclusionsThe significant increase of TIA1‐positive IELs in duodenal tissue specimens is associated with FA. The cytotoxicity of T lymphocytes seems to play a role in the pathogenesis of gastrointestinal FA. Activation and mechanisms of action should be studied further.

Publisher

Wiley

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