Role of Suppressor of cytokine signaling 2 during the development and resolution of an experimental arthritis.
Cramer, A
Galvão, I
Venturini de Sá, N
Gaio, P
Fernanda de Melo Oliveira, N
Rates Gonzaga Santos, M
Henrique Campolina-Silva, G
Vinicius Santos Valiate, B
Rezende Souza, F
Dantas Cassali, G
Martins Teixeira, M
Almeida Amaral, F
Simão Machado, F
- Publisher:
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Publication Type:
- Journal Article
- Citation:
- Cell Immunol, 2022, 372, pp. 104476
- Issue Date:
- 2022-02
Closed Access
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1-s2.0-S0008874921001970-main.pdf | 12.04 MB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Cramer, A | |
dc.contributor.author | Galvão, I | |
dc.contributor.author | Venturini de Sá, N | |
dc.contributor.author | Gaio, P | |
dc.contributor.author | Fernanda de Melo Oliveira, N | |
dc.contributor.author | Rates Gonzaga Santos, M | |
dc.contributor.author | Henrique Campolina-Silva, G | |
dc.contributor.author | Vinicius Santos Valiate, B | |
dc.contributor.author | Rezende Souza, F | |
dc.contributor.author | Dantas Cassali, G | |
dc.contributor.author | Martins Teixeira, M | |
dc.contributor.author | Almeida Amaral, F | |
dc.contributor.author | Simão Machado, F | |
dc.date.accessioned | 2023-02-06T03:29:44Z | |
dc.date.available | 2021-12-31 | |
dc.date.available | 2023-02-06T03:29:44Z | |
dc.date.issued | 2022-02 | |
dc.identifier.citation | Cell Immunol, 2022, 372, pp. 104476 | |
dc.identifier.issn | 0008-8749 | |
dc.identifier.issn | 1090-2163 | |
dc.identifier.uri | http://hdl.handle.net/10453/165935 | |
dc.description.abstract | Rheumatoid arthritis(RA) is a debilitating chronic inflammatory disease. Suppressors of Cytokine Signaling(SOCS) proteins regulate homeostasis and pathogenesis in several diseases. The intersection between RA pathophysiology and SOCS2 is unclear. Herein, we investigated the roles of SOCS2 during the development of an experimental antigen-induced arthritis(AIA). In wild type mice, joint SOCS2 expression was reduced during AIA development. At the peak of inflammation, SOCS2-/- mice presented with reduced numbers of infiltrated cells in their joints. At the late phase of AIA, however, exhibited increased adhesion/infiltration of neutrophils, macrophages, CD4+-T cells, CD4+CD8+-T cells, and CD4-CD8--T cells associated with elevated IL-17 and IFN-γ levels, joint damage, proteoglycan loss, and nociception. SOCS2 deficiency resulted in lower numbers of apoptotic neutrophils and reduced efferocytosis. The present study demonstrated the vital role of SOCS2 during the development and resolution of an experimental RA model. Hence, this protein may be a novel therapeutic target for this disorder. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | |
dc.relation.ispartof | Cell Immunol | |
dc.relation.isbasedon | 10.1016/j.cellimm.2021.104476 | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject | 1107 Immunology | |
dc.subject.classification | Immunology | |
dc.subject.mesh | Adaptive Immunity | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Arthritis, Experimental | |
dc.subject.mesh | Cell Adhesion | |
dc.subject.mesh | Disease Progression | |
dc.subject.mesh | Endocytosis | |
dc.subject.mesh | Immunity, Innate | |
dc.subject.mesh | Leukocytes | |
dc.subject.mesh | Macrophages | |
dc.subject.mesh | Male | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Mice, Knockout | |
dc.subject.mesh | Spleen | |
dc.subject.mesh | Suppressor of Cytokine Signaling Proteins | |
dc.subject.mesh | Spleen | |
dc.subject.mesh | Leukocytes | |
dc.subject.mesh | Macrophages | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Mice, Knockout | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Arthritis, Experimental | |
dc.subject.mesh | Disease Progression | |
dc.subject.mesh | Cell Adhesion | |
dc.subject.mesh | Endocytosis | |
dc.subject.mesh | Male | |
dc.subject.mesh | Suppressor of Cytokine Signaling Proteins | |
dc.subject.mesh | Immunity, Innate | |
dc.subject.mesh | Adaptive Immunity | |
dc.title | Role of Suppressor of cytokine signaling 2 during the development and resolution of an experimental arthritis. | |
dc.type | Journal Article | |
utslib.citation.volume | 372 | |
utslib.location.activity | Netherlands | |
utslib.for | 1107 Immunology | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | closed_access | * |
dc.date.updated | 2023-02-06T03:29:42Z | |
pubs.publication-status | Published | |
pubs.volume | 372 |
Abstract:
Rheumatoid arthritis(RA) is a debilitating chronic inflammatory disease. Suppressors of Cytokine Signaling(SOCS) proteins regulate homeostasis and pathogenesis in several diseases. The intersection between RA pathophysiology and SOCS2 is unclear. Herein, we investigated the roles of SOCS2 during the development of an experimental antigen-induced arthritis(AIA). In wild type mice, joint SOCS2 expression was reduced during AIA development. At the peak of inflammation, SOCS2-/- mice presented with reduced numbers of infiltrated cells in their joints. At the late phase of AIA, however, exhibited increased adhesion/infiltration of neutrophils, macrophages, CD4+-T cells, CD4+CD8+-T cells, and CD4-CD8--T cells associated with elevated IL-17 and IFN-γ levels, joint damage, proteoglycan loss, and nociception. SOCS2 deficiency resulted in lower numbers of apoptotic neutrophils and reduced efferocytosis. The present study demonstrated the vital role of SOCS2 during the development and resolution of an experimental RA model. Hence, this protein may be a novel therapeutic target for this disorder.
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