Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease
- Autores
- Pérez, Federico; Ruera, Carolina Naymé; Miculán, Emanuel Gonzalo; Carasi, Paula; Chirdo, Fernando Gabriel
- Año de publicación
- 2021
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- The small intestine has a high rate of cell turnover under homeostatic conditions, and this increases further in response to infection or damage. Epithelial cells mostly die by apoptosis, but recent studies indicate that this may also involve pro-inflammatory pathways of programmed cell death, such as pyroptosis and necroptosis. Celiac disease (CD), the most prevalent immune-based enteropathy, is caused by loss of oral tolerance to peptides derived from wheat, rye, and barley in genetically predisposed individuals. Although cytotoxic cells and gluten-specific CD4+ Th1 cells are the central players in the pathology, inflammatory pathways induced by cell death may participate in driving and sustaining the disease through the release of alarmins. In this review, we summarize the recent literature addressing the role of programmed cell death pathways in the small intestine, describing how these mechanisms may contribute to CD and discussing their potential implications.
Instituto de Estudios Inmunológicos y Fisiopatológicos - Materia
-
Biología
Celiac disease
Alarmins
Programmed cell death
Inflammation
Small intestine - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/125443
Ver los metadatos del registro completo
id |
SEDICI_08ecef7305b657d48acaf50bb2a35fd9 |
---|---|
oai_identifier_str |
oai:sedici.unlp.edu.ar:10915/125443 |
network_acronym_str |
SEDICI |
repository_id_str |
1329 |
network_name_str |
SEDICI (UNLP) |
spelling |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac DiseasePérez, FedericoRuera, Carolina NayméMiculán, Emanuel GonzaloCarasi, PaulaChirdo, Fernando GabrielBiologíaCeliac diseaseAlarminsProgrammed cell deathInflammationSmall intestineThe small intestine has a high rate of cell turnover under homeostatic conditions, and this increases further in response to infection or damage. Epithelial cells mostly die by apoptosis, but recent studies indicate that this may also involve pro-inflammatory pathways of programmed cell death, such as pyroptosis and necroptosis. Celiac disease (CD), the most prevalent immune-based enteropathy, is caused by loss of oral tolerance to peptides derived from wheat, rye, and barley in genetically predisposed individuals. Although cytotoxic cells and gluten-specific CD4+ Th1 cells are the central players in the pathology, inflammatory pathways induced by cell death may participate in driving and sustaining the disease through the release of alarmins. In this review, we summarize the recent literature addressing the role of programmed cell death pathways in the small intestine, describing how these mechanisms may contribute to CD and discussing their potential implications.Instituto de Estudios Inmunológicos y Fisiopatológicos2021info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/125443enginfo:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/22/14/7426info:eu-repo/semantics/altIdentifier/issn/1422-0067info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms22147426info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-17T10:12:48Zoai:sedici.unlp.edu.ar:10915/125443Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-17 10:12:48.334SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease |
title |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease |
spellingShingle |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease Pérez, Federico Biología Celiac disease Alarmins Programmed cell death Inflammation Small intestine |
title_short |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease |
title_full |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease |
title_fullStr |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease |
title_full_unstemmed |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease |
title_sort |
Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease |
dc.creator.none.fl_str_mv |
Pérez, Federico Ruera, Carolina Naymé Miculán, Emanuel Gonzalo Carasi, Paula Chirdo, Fernando Gabriel |
author |
Pérez, Federico |
author_facet |
Pérez, Federico Ruera, Carolina Naymé Miculán, Emanuel Gonzalo Carasi, Paula Chirdo, Fernando Gabriel |
author_role |
author |
author2 |
Ruera, Carolina Naymé Miculán, Emanuel Gonzalo Carasi, Paula Chirdo, Fernando Gabriel |
author2_role |
author author author author |
dc.subject.none.fl_str_mv |
Biología Celiac disease Alarmins Programmed cell death Inflammation Small intestine |
topic |
Biología Celiac disease Alarmins Programmed cell death Inflammation Small intestine |
dc.description.none.fl_txt_mv |
The small intestine has a high rate of cell turnover under homeostatic conditions, and this increases further in response to infection or damage. Epithelial cells mostly die by apoptosis, but recent studies indicate that this may also involve pro-inflammatory pathways of programmed cell death, such as pyroptosis and necroptosis. Celiac disease (CD), the most prevalent immune-based enteropathy, is caused by loss of oral tolerance to peptides derived from wheat, rye, and barley in genetically predisposed individuals. Although cytotoxic cells and gluten-specific CD4+ Th1 cells are the central players in the pathology, inflammatory pathways induced by cell death may participate in driving and sustaining the disease through the release of alarmins. In this review, we summarize the recent literature addressing the role of programmed cell death pathways in the small intestine, describing how these mechanisms may contribute to CD and discussing their potential implications. Instituto de Estudios Inmunológicos y Fisiopatológicos |
description |
The small intestine has a high rate of cell turnover under homeostatic conditions, and this increases further in response to infection or damage. Epithelial cells mostly die by apoptosis, but recent studies indicate that this may also involve pro-inflammatory pathways of programmed cell death, such as pyroptosis and necroptosis. Celiac disease (CD), the most prevalent immune-based enteropathy, is caused by loss of oral tolerance to peptides derived from wheat, rye, and barley in genetically predisposed individuals. Although cytotoxic cells and gluten-specific CD4+ Th1 cells are the central players in the pathology, inflammatory pathways induced by cell death may participate in driving and sustaining the disease through the release of alarmins. In this review, we summarize the recent literature addressing the role of programmed cell death pathways in the small intestine, describing how these mechanisms may contribute to CD and discussing their potential implications. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion Articulo 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://sedici.unlp.edu.ar/handle/10915/125443 |
url |
http://sedici.unlp.edu.ar/handle/10915/125443 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/22/14/7426 info:eu-repo/semantics/altIdentifier/issn/1422-0067 info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms22147426 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
dc.format.none.fl_str_mv |
application/pdf |
dc.source.none.fl_str_mv |
reponame:SEDICI (UNLP) instname:Universidad Nacional de La Plata instacron:UNLP |
reponame_str |
SEDICI (UNLP) |
collection |
SEDICI (UNLP) |
instname_str |
Universidad Nacional de La Plata |
instacron_str |
UNLP |
institution |
UNLP |
repository.name.fl_str_mv |
SEDICI (UNLP) - Universidad Nacional de La Plata |
repository.mail.fl_str_mv |
alira@sedici.unlp.edu.ar |
_version_ |
1843532746734960640 |
score |
13.004268 |