Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice

Autores
Chen, Lili; Deshpande, Madhura; Grisotto, Marcos; Smaldini, Paola Lorena; Garcia, Roberto; He, Zhengxiang; Gulko, Percio; Lira, Sergio A.; Furtado, Glaucia C.
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Psoriasis (PS) is a chronic skin inflammation. Up to 30% of the patients with PS develop psoriatic arthritis (PsA), a condition characterized by inflammatory arthritis that affects joints or entheses. Although there is mounting evidence for a critical role of interleukin-23 (IL-23) signaling in the pathogenesis of both PS and PsA, it remains unclear whether IL-23-induced skin inflammation drives joint disease. Here, we show that mice expressing increased levels of IL-23 in the skin (K23 mice) develop a PS-like disease that is characterized by acanthosis, parakeratosis, hyperkeratosis, and inflammatory infiltrates in the dermis. Skin disease preceded development of PsA, including enthesitis, dactylitis, and bone destruction. The development of enthesitis and dactylitis was not due to high circulating levels of IL-23, as transgenic animals and controls had similar levels of this cytokine in circulation. IL-22, a downstream cytokine of IL-23, was highly increased in the serum of K23 mice. Although IL-22 deficiency did not affect skin disease development, IL-22 deficiency aggravated the PsA-like disease in K23 mice. Our results demonstrate a central role for skin expressed IL-23 in the initiation of PS and on pathogenic processes leading to PsA.
Fil: Chen, Lili. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Deshpande, Madhura. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Grisotto, Marcos. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Smaldini, Paola Lorena. Icahn School of Medicine at Mount Sinai; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Estudios Inmunológicos y Fisiopatológicos. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Instituto de Estudios Inmunológicos y Fisiopatológicos; Argentina
Fil: Garcia, Roberto. Hospital for Special Surgery; Estados Unidos
Fil: He, Zhengxiang. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Gulko, Percio. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Lira, Sergio A.. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Furtado, Glaucia C.. Icahn School of Medicine at Mount Sinai; Estados Unidos
Materia
IL-23
PSORIATIC-ARTHRITIS
IL-22
INFLAMMATION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/155930
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/155930
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in miceChen, LiliDeshpande, MadhuraGrisotto, MarcosSmaldini, Paola LorenaGarcia, RobertoHe, ZhengxiangGulko, PercioLira, Sergio A.Furtado, Glaucia C.IL-23PSORIATIC-ARTHRITISIL-22INFLAMMATIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Psoriasis (PS) is a chronic skin inflammation. Up to 30% of the patients with PS develop psoriatic arthritis (PsA), a condition characterized by inflammatory arthritis that affects joints or entheses. Although there is mounting evidence for a critical role of interleukin-23 (IL-23) signaling in the pathogenesis of both PS and PsA, it remains unclear whether IL-23-induced skin inflammation drives joint disease. Here, we show that mice expressing increased levels of IL-23 in the skin (K23 mice) develop a PS-like disease that is characterized by acanthosis, parakeratosis, hyperkeratosis, and inflammatory infiltrates in the dermis. Skin disease preceded development of PsA, including enthesitis, dactylitis, and bone destruction. The development of enthesitis and dactylitis was not due to high circulating levels of IL-23, as transgenic animals and controls had similar levels of this cytokine in circulation. IL-22, a downstream cytokine of IL-23, was highly increased in the serum of K23 mice. Although IL-22 deficiency did not affect skin disease development, IL-22 deficiency aggravated the PsA-like disease in K23 mice. Our results demonstrate a central role for skin expressed IL-23 in the initiation of PS and on pathogenic processes leading to PsA.Fil: Chen, Lili. Icahn School of Medicine at Mount Sinai; Estados UnidosFil: Deshpande, Madhura. Icahn School of Medicine at Mount Sinai; Estados UnidosFil: Grisotto, Marcos. Icahn School of Medicine at Mount Sinai; Estados UnidosFil: Smaldini, Paola Lorena. Icahn School of Medicine at Mount Sinai; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Estudios Inmunológicos y Fisiopatológicos. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Instituto de Estudios Inmunológicos y Fisiopatológicos; ArgentinaFil: Garcia, Roberto. Hospital for Special Surgery; Estados UnidosFil: He, Zhengxiang. Icahn School of Medicine at Mount Sinai; Estados UnidosFil: Gulko, Percio. Icahn School of Medicine at Mount Sinai; Estados UnidosFil: Lira, Sergio A.. Icahn School of Medicine at Mount Sinai; Estados UnidosFil: Furtado, Glaucia C.. Icahn School of Medicine at Mount Sinai; Estados UnidosNature Publishing Group2020-05-19info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/155930Chen, Lili; Deshpande, Madhura; Grisotto, Marcos; Smaldini, Paola Lorena; Garcia, Roberto; et al.; Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice; Nature Publishing Group; Scientific Reports; 10; 19-5-2020; 1-112045-2322CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-020-65269-6info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41598-020-65269-6info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:02:03Zoai:ri.conicet.gov.ar:11336/155930instacron: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 10:02:03.525CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
title Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
spellingShingle Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
Chen, Lili
IL-23
PSORIATIC-ARTHRITIS
IL-22
INFLAMMATION
title_short Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
title_full Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
title_fullStr Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
title_full_unstemmed Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
title_sort Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice
dc.creator.none.fl_str_mv Chen, Lili
Deshpande, Madhura
Grisotto, Marcos
Smaldini, Paola Lorena
Garcia, Roberto
He, Zhengxiang
Gulko, Percio
Lira, Sergio A.
Furtado, Glaucia C.
author Chen, Lili
author_facet Chen, Lili
Deshpande, Madhura
Grisotto, Marcos
Smaldini, Paola Lorena
Garcia, Roberto
He, Zhengxiang
Gulko, Percio
Lira, Sergio A.
Furtado, Glaucia C.
author_role author
author2 Deshpande, Madhura
Grisotto, Marcos
Smaldini, Paola Lorena
Garcia, Roberto
He, Zhengxiang
Gulko, Percio
Lira, Sergio A.
Furtado, Glaucia C.
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv IL-23
PSORIATIC-ARTHRITIS
IL-22
INFLAMMATION
topic IL-23
PSORIATIC-ARTHRITIS
IL-22
INFLAMMATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Psoriasis (PS) is a chronic skin inflammation. Up to 30% of the patients with PS develop psoriatic arthritis (PsA), a condition characterized by inflammatory arthritis that affects joints or entheses. Although there is mounting evidence for a critical role of interleukin-23 (IL-23) signaling in the pathogenesis of both PS and PsA, it remains unclear whether IL-23-induced skin inflammation drives joint disease. Here, we show that mice expressing increased levels of IL-23 in the skin (K23 mice) develop a PS-like disease that is characterized by acanthosis, parakeratosis, hyperkeratosis, and inflammatory infiltrates in the dermis. Skin disease preceded development of PsA, including enthesitis, dactylitis, and bone destruction. The development of enthesitis and dactylitis was not due to high circulating levels of IL-23, as transgenic animals and controls had similar levels of this cytokine in circulation. IL-22, a downstream cytokine of IL-23, was highly increased in the serum of K23 mice. Although IL-22 deficiency did not affect skin disease development, IL-22 deficiency aggravated the PsA-like disease in K23 mice. Our results demonstrate a central role for skin expressed IL-23 in the initiation of PS and on pathogenic processes leading to PsA.
Fil: Chen, Lili. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Deshpande, Madhura. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Grisotto, Marcos. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Smaldini, Paola Lorena. Icahn School of Medicine at Mount Sinai; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Estudios Inmunológicos y Fisiopatológicos. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Instituto de Estudios Inmunológicos y Fisiopatológicos; Argentina
Fil: Garcia, Roberto. Hospital for Special Surgery; Estados Unidos
Fil: He, Zhengxiang. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Gulko, Percio. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Lira, Sergio A.. Icahn School of Medicine at Mount Sinai; Estados Unidos
Fil: Furtado, Glaucia C.. Icahn School of Medicine at Mount Sinai; Estados Unidos
description Psoriasis (PS) is a chronic skin inflammation. Up to 30% of the patients with PS develop psoriatic arthritis (PsA), a condition characterized by inflammatory arthritis that affects joints or entheses. Although there is mounting evidence for a critical role of interleukin-23 (IL-23) signaling in the pathogenesis of both PS and PsA, it remains unclear whether IL-23-induced skin inflammation drives joint disease. Here, we show that mice expressing increased levels of IL-23 in the skin (K23 mice) develop a PS-like disease that is characterized by acanthosis, parakeratosis, hyperkeratosis, and inflammatory infiltrates in the dermis. Skin disease preceded development of PsA, including enthesitis, dactylitis, and bone destruction. The development of enthesitis and dactylitis was not due to high circulating levels of IL-23, as transgenic animals and controls had similar levels of this cytokine in circulation. IL-22, a downstream cytokine of IL-23, was highly increased in the serum of K23 mice. Although IL-22 deficiency did not affect skin disease development, IL-22 deficiency aggravated the PsA-like disease in K23 mice. Our results demonstrate a central role for skin expressed IL-23 in the initiation of PS and on pathogenic processes leading to PsA.
publishDate 2020
dc.date.none.fl_str_mv 2020-05-19
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/11336/155930
Chen, Lili; Deshpande, Madhura; Grisotto, Marcos; Smaldini, Paola Lorena; Garcia, Roberto; et al.; Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice; Nature Publishing Group; Scientific Reports; 10; 19-5-2020; 1-11
2045-2322
CONICET Digital
CONICET
url http://hdl.handle.net/11336/155930
identifier_str_mv Chen, Lili; Deshpande, Madhura; Grisotto, Marcos; Smaldini, Paola Lorena; Garcia, Roberto; et al.; Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice; Nature Publishing Group; Scientific Reports; 10; 19-5-2020; 1-11
2045-2322
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-020-65269-6
info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41598-020-65269-6
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Nature Publishing Group
publisher.none.fl_str_mv Nature Publishing Group
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
_version_ 1842269734176817152
score 13.13397

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