Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice
- Autores
- Galipeau, Heather J.; Rulli, Nestor Ezequiel; Jury, Jennifer; Huang, Xianxi; Araya, Romina Elizabeth; Murray, Joseph A.; David, Chella S.; Chirdo, Fernando Gabriel; McCoy, Kathy D.; Verdu, Elena F.
- Año de publicación
- 2011
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Celiac Disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit antibodies against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to play a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed mucosal dysfunction, but no insulitis. Administration of anti-CD25 mAbs before sensitization induced partial depletion of CD25+Foxp3+ T-cells and led to insulitis. Mice that developed insulitis had increased pro-inflammatory cytokines in the mesenteric (MLN) and pancreatic lymph nodes (PLN). CD4+ T-cells isolated from PLN of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubations with gliadin but not, with bovine serum albumin (BSA). In control mice, CD4+ T-cells from PLN did not proliferate in response to gliadin. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice but insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T-cells. This animal model provides a mechanistic link through which the dietary antigen gliadin, which triggers CD, modulates the onset of insulitis in the presence of partial regulatory T cell deficiency. Both innate and adaptive immune mechanisms related to gluten intolerance can be investigated in NOD-DQ8 mice.
Fil: Galipeau, Heather J.. McMaster University Medical Centre; Canadá
Fil: Rulli, Nestor Ezequiel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina
Fil: Jury, Jennifer. McMaster University Medical Centre; Canadá
Fil: Huang, Xianxi. McMaster University Medical Centre; Canadá
Fil: Araya, Romina Elizabeth. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina
Fil: Murray, Joseph A.. Mayo Clinic Cancer Center; Estados Unidos
Fil: David, Chella S.. Mayo Clinic Cancer Center; Estados Unidos
Fil: Chirdo, Fernando Gabriel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina
Fil: McCoy, Kathy D.. McMaster University Medical Centre; Canadá
Fil: Verdu, Elena F.. McMaster University Medical Centre; Canadá - Materia
-
INTESTINE
DIABETES
INNATE IMMUNITY - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/105196
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Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 miceGalipeau, Heather J.Rulli, Nestor EzequielJury, JenniferHuang, XianxiAraya, Romina ElizabethMurray, Joseph A.David, Chella S.Chirdo, Fernando GabrielMcCoy, Kathy D.Verdu, Elena F.INTESTINEDIABETESINNATE IMMUNITYhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Celiac Disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit antibodies against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to play a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed mucosal dysfunction, but no insulitis. Administration of anti-CD25 mAbs before sensitization induced partial depletion of CD25+Foxp3+ T-cells and led to insulitis. Mice that developed insulitis had increased pro-inflammatory cytokines in the mesenteric (MLN) and pancreatic lymph nodes (PLN). CD4+ T-cells isolated from PLN of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubations with gliadin but not, with bovine serum albumin (BSA). In control mice, CD4+ T-cells from PLN did not proliferate in response to gliadin. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice but insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T-cells. This animal model provides a mechanistic link through which the dietary antigen gliadin, which triggers CD, modulates the onset of insulitis in the presence of partial regulatory T cell deficiency. Both innate and adaptive immune mechanisms related to gluten intolerance can be investigated in NOD-DQ8 mice.Fil: Galipeau, Heather J.. McMaster University Medical Centre; CanadáFil: Rulli, Nestor Ezequiel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Jury, Jennifer. McMaster University Medical Centre; CanadáFil: Huang, Xianxi. McMaster University Medical Centre; CanadáFil: Araya, Romina Elizabeth. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Murray, Joseph A.. Mayo Clinic Cancer Center; Estados UnidosFil: David, Chella S.. Mayo Clinic Cancer Center; Estados UnidosFil: Chirdo, Fernando Gabriel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: McCoy, Kathy D.. McMaster University Medical Centre; CanadáFil: Verdu, Elena F.. McMaster University Medical Centre; CanadáAmerican Association of Immunologists2011-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/105196Galipeau, Heather J.; Rulli, Nestor Ezequiel; Jury, Jennifer; Huang, Xianxi; Araya, Romina Elizabeth; et al.; Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice; American Association of Immunologists; Journal of Immunology; 187; 8; 10-2011; 4338-43460022-1767CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.1100854info:eu-repo/semantics/altIdentifier/url/https://www.jimmunol.org/content/187/8/4338info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:51:15Zoai:ri.conicet.gov.ar:11336/105196instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:51:15.301CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice |
title |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice |
spellingShingle |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice Galipeau, Heather J. INTESTINE DIABETES INNATE IMMUNITY |
title_short |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice |
title_full |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice |
title_fullStr |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice |
title_full_unstemmed |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice |
title_sort |
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice |
dc.creator.none.fl_str_mv |
Galipeau, Heather J. Rulli, Nestor Ezequiel Jury, Jennifer Huang, Xianxi Araya, Romina Elizabeth Murray, Joseph A. David, Chella S. Chirdo, Fernando Gabriel McCoy, Kathy D. Verdu, Elena F. |
author |
Galipeau, Heather J. |
author_facet |
Galipeau, Heather J. Rulli, Nestor Ezequiel Jury, Jennifer Huang, Xianxi Araya, Romina Elizabeth Murray, Joseph A. David, Chella S. Chirdo, Fernando Gabriel McCoy, Kathy D. Verdu, Elena F. |
author_role |
author |
author2 |
Rulli, Nestor Ezequiel Jury, Jennifer Huang, Xianxi Araya, Romina Elizabeth Murray, Joseph A. David, Chella S. Chirdo, Fernando Gabriel McCoy, Kathy D. Verdu, Elena F. |
author2_role |
author author author author author author author author author |
dc.subject.none.fl_str_mv |
INTESTINE DIABETES INNATE IMMUNITY |
topic |
INTESTINE DIABETES INNATE IMMUNITY |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Celiac Disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit antibodies against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to play a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed mucosal dysfunction, but no insulitis. Administration of anti-CD25 mAbs before sensitization induced partial depletion of CD25+Foxp3+ T-cells and led to insulitis. Mice that developed insulitis had increased pro-inflammatory cytokines in the mesenteric (MLN) and pancreatic lymph nodes (PLN). CD4+ T-cells isolated from PLN of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubations with gliadin but not, with bovine serum albumin (BSA). In control mice, CD4+ T-cells from PLN did not proliferate in response to gliadin. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice but insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T-cells. This animal model provides a mechanistic link through which the dietary antigen gliadin, which triggers CD, modulates the onset of insulitis in the presence of partial regulatory T cell deficiency. Both innate and adaptive immune mechanisms related to gluten intolerance can be investigated in NOD-DQ8 mice. Fil: Galipeau, Heather J.. McMaster University Medical Centre; Canadá Fil: Rulli, Nestor Ezequiel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina Fil: Jury, Jennifer. McMaster University Medical Centre; Canadá Fil: Huang, Xianxi. McMaster University Medical Centre; Canadá Fil: Araya, Romina Elizabeth. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina Fil: Murray, Joseph A.. Mayo Clinic Cancer Center; Estados Unidos Fil: David, Chella S.. Mayo Clinic Cancer Center; Estados Unidos Fil: Chirdo, Fernando Gabriel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina Fil: McCoy, Kathy D.. McMaster University Medical Centre; Canadá Fil: Verdu, Elena F.. McMaster University Medical Centre; Canadá |
description |
Celiac Disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit antibodies against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to play a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed mucosal dysfunction, but no insulitis. Administration of anti-CD25 mAbs before sensitization induced partial depletion of CD25+Foxp3+ T-cells and led to insulitis. Mice that developed insulitis had increased pro-inflammatory cytokines in the mesenteric (MLN) and pancreatic lymph nodes (PLN). CD4+ T-cells isolated from PLN of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubations with gliadin but not, with bovine serum albumin (BSA). In control mice, CD4+ T-cells from PLN did not proliferate in response to gliadin. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice but insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T-cells. This animal model provides a mechanistic link through which the dietary antigen gliadin, which triggers CD, modulates the onset of insulitis in the presence of partial regulatory T cell deficiency. Both innate and adaptive immune mechanisms related to gluten intolerance can be investigated in NOD-DQ8 mice. |
publishDate |
2011 |
dc.date.none.fl_str_mv |
2011-10 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/105196 Galipeau, Heather J.; Rulli, Nestor Ezequiel; Jury, Jennifer; Huang, Xianxi; Araya, Romina Elizabeth; et al.; Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice; American Association of Immunologists; Journal of Immunology; 187; 8; 10-2011; 4338-4346 0022-1767 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/105196 |
identifier_str_mv |
Galipeau, Heather J.; Rulli, Nestor Ezequiel; Jury, Jennifer; Huang, Xianxi; Araya, Romina Elizabeth; et al.; Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice; American Association of Immunologists; Journal of Immunology; 187; 8; 10-2011; 4338-4346 0022-1767 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.1100854 info:eu-repo/semantics/altIdentifier/url/https://www.jimmunol.org/content/187/8/4338 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
American Association of Immunologists |
publisher.none.fl_str_mv |
American Association of Immunologists |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
reponame_str |
CONICET Digital (CONICET) |
collection |
CONICET Digital (CONICET) |
instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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1842269083099201536 |
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13.13397 |