Publication: Duodenal mucosa FOXP3 expression in different etiologies of lymphocytic duodenosis
Authors
Vaquero, Luis ; Rodríguez Martín, Laura ; Hernando, Mercedes ; Jiménez, Marcos ; Monteserín, Luz ; Alvarez Cuenllas, Begoña ; Ruiz de Morales, José M. ; Calleja, Sara ; Vivas, Santiago
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-11-888
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info:eu-repo/semantics/article
Description
Abstract
Background/aims. In celiac disease there is
an increase of lymphocytes expressing FOXP3 in the
intestinal mucosa associated with varying degrees of
villous atrophy. Our aim was to evaluate FOXP3
expression in duodenal mucosa with lymphocytic
enteritis according to aetiology and correlation with
lymphocytes T- γδ.
Methods. We compared three adult patient groups
suffering lymphocytic enteritis: celiacs following a
gluten-free diet (n=12), first-degree relatives of celiac
patients with genetic risks (n=14) and patients with
functional dyspepsia (n=14), along with a control group
not suffering from duodenal enteritis (n=16). The
population of duodenal lymphocytes was analysed by
immunohistochemistry assays for CD3+ characterisation
and FOXP3 expression. Quantification of lymphocytes
T-γδ in duodenal mucosa was performed by flow
cytometry in fresh tissue samples.
Results. Presence of lymphocytes T-γδ was
significantly higher in the group of celiac individuals
compared to the group of relatives of these individuals
(37.44 vs 5,52: p<0.0001) and the group with functional
dyspepsia (37.44 vs 11.76: p=0.008). FOXP3 expression
was also significantly higher in the celiac group than in
the groups of relatives (18.85 vs 6.31; p=0.001) and
functional dyspepsia patients (18.85 vs 7.61; p=0.023).
The proportion of lymphocytes T-γδ and FOXP3-
expressing lymphocytes was similar in the control group
to that in the relatives or functional dyspepsia groups.
Conclusions. Lymphocytic enteritis associated to
celiac disease shows an increase of FOXP3 expression
and lymphocytes T- γδ that is not detected in other
etiologies of enteritis.
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Citation
Histology and Histopathology, Vol.33, nº1, (2018)
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