Basal lamina disorganisation of the acini and ducts of labial salivary glands from patients with Sjogren's syndrome:: association with mononuclear cell infiltration
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Archivos
Fecha
2006-02-01
Profesor/a Guía
Facultad/escuela
Idioma
en
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BMJ PUBLISHING GROUP
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Licencia CC
CC BY-NC 4.0
ATRIBUCIÓN-NOCOMERCIAL 4.0 INTERNACIONAL
Deed
Licencia CC
https://creativecommons.org/licenses/by-nc/4.0/deed.es
Resumen
Objective: To study the expression of laminin and type IV collagen as biomarkers of the organisation of the basal lamina of acini and ducts in labial salivary glands from patients with Sjogren's syndrome, and to relate this organisation to inflammatory cell invasion of acini and ducts.
Methods: Immunohistochemistry for laminin and type IV collagen was undertaken on sections of labial salivary glands from 30 patients with Sjogren's syndrome, 10 control subjects, and 24 controls with chronic sialoadenitis. Immunohistochemistry reaction, alterations to cell morphology, and the presence of inflammatory cells in acini and ducts were evaluated and scored using a semiquantitative method.
Results: Changes in the expression of laminin and type IV collagen in the basal lamina of acini and ducts of labial salivary glands from patients with Sjogren's syndrome were more pronounced than in labial salivary glands from control groups. A remarkable characteristic was the disorganisation of the basal lamina in the labial salivary glands in Sjogren's syndrome. The pattern of immunoreactivity of the basal lamina of other structures (for example, blood vessels) did not change. In Sjogren's syndrome, invasion of cytotoxic T lymphocytes was only observed in acini and ducts which had a disorganised basal lamina.
Conclusions: The high state of disorganisation of the basal lamina of acini and ducts could allow invasion of cytotoxic T lymphocytes in Sjogren's syndrome, contributing to cell death and ductal hyperplasia.
Notas
INDEXACIÓN: WEB OF SCIENCE.
Palabras clave
MESSENGER-RNA EXPRESSION, NOD MOUSE MODEL, MATRIX METALLOPROTEINASES, LYMPHOCYTIC INFILTRATION, TRANSCRIPTION FACTORS, PATHOGENESIS, DESTRUCTION, MECHANISMS, ARTHRITIS, PROTEINS
Citación
ANNALS OF THE RHEUMATIC DISEASES, Volume 65, Issue 2, Page 178-183
DOI
10.1136/ard.2004.033837