Role of CXCR3/CXCL10 axis in immune cell recruitment into the small intestine in celiac disease

Lymphocytic infiltration in the lamina propria (LP), which is primarily composed of CD4+ Th1 cells and plasma cells, and increased numbers of intraepithelial lymphocytes (IELs), is a characteristic finding in active celiac disease (CD). Signals for this selective cell recruitment have not been fully...

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Autores principales: Bondar, Constanza María, Araya, Romina Elizabeth, Guzman, Luciana, Cueto Rua, Eduardo, Chopita, Néstor Alfredo, Chirdo, Fernando Gabriel
Formato: Articulo
Lenguaje:Inglés
Publicado: 2014
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Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/85562
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id I19-R120-10915-85562
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Exactas
Enfermedad Celíaca
spellingShingle Ciencias Exactas
Enfermedad Celíaca
Bondar, Constanza María
Araya, Romina Elizabeth
Guzman, Luciana
Cueto Rua, Eduardo
Chopita, Néstor Alfredo
Chirdo, Fernando Gabriel
Role of CXCR3/CXCL10 axis in immune cell recruitment into the small intestine in celiac disease
topic_facet Ciencias Exactas
Enfermedad Celíaca
description Lymphocytic infiltration in the lamina propria (LP), which is primarily composed of CD4+ Th1 cells and plasma cells, and increased numbers of intraepithelial lymphocytes (IELs), is a characteristic finding in active celiac disease (CD). Signals for this selective cell recruitment have not been fully established. CXCR3 and its ligands, particularly CXCL10, have been suggested to be one of the most relevant pathways in the attraction of cells into inflamed tissues. In addition, CXCR3 is characteristically expressed by Th1 cells. The aim of this work was to investigate the participation of the chemokine CXCL10/CXCR3 axis in CD pathogenesis. A higher concentration of CXCL10 was found in the serum of untreated CD patients. The mRNA levels of CXCL10 and CXCL11 but not CXCL9 were significantly higher in duodenal biopsies from untreated CD patients compared with non-CD controls or treated patients. The results demonstrate that CXCL10 is abundantly produced in untreated CD and reduced in treated patients, and the expression of CXCL10 was found to be correlated with the IFNγ levels in the tissue. Plasma cells and enterocytes were identified as CXCL10-producing cells. Moreover, the CXCL10 expression in intestinal tissues was upregulated by poly I:C and IL-15. IELs, LP T lymphocytes, and plasma cells, which infiltrate the intestinal mucosa in untreated CD, express CXCR3. The CXCR3/CXCL10 signalling axis is overactivated in the small intestinal mucosa in untreated patients, and this finding explains the specific recruitment of the major cell populations that infiltrate the epithelium and the LP in CD.
format Articulo
Articulo
author Bondar, Constanza María
Araya, Romina Elizabeth
Guzman, Luciana
Cueto Rua, Eduardo
Chopita, Néstor Alfredo
Chirdo, Fernando Gabriel
author_facet Bondar, Constanza María
Araya, Romina Elizabeth
Guzman, Luciana
Cueto Rua, Eduardo
Chopita, Néstor Alfredo
Chirdo, Fernando Gabriel
author_sort Bondar, Constanza María
title Role of CXCR3/CXCL10 axis in immune cell recruitment into the small intestine in celiac disease
title_short Role of CXCR3/CXCL10 axis in immune cell recruitment into the small intestine in celiac disease
title_full Role of CXCR3/CXCL10 axis in immune cell recruitment into the small intestine in celiac disease
title_fullStr Role of CXCR3/CXCL10 axis in immune cell recruitment into the small intestine in celiac disease
title_full_unstemmed Role of CXCR3/CXCL10 axis in immune cell recruitment into the small intestine in celiac disease
title_sort role of cxcr3/cxcl10 axis in immune cell recruitment into the small intestine in celiac disease
publishDate 2014
url http://sedici.unlp.edu.ar/handle/10915/85562
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AT arayarominaelizabeth roleofcxcr3cxcl10axisinimmunecellrecruitmentintothesmallintestineinceliacdisease
AT guzmanluciana roleofcxcr3cxcl10axisinimmunecellrecruitmentintothesmallintestineinceliacdisease
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