C17 prevents inflammatory arthritis and associated joint destruction in mice.

C17 was first described about ten years ago as a gene expressed in CD34+ cells. A more recent study has suggested a role for C17 in chondrogenesis and development of cartilage. However, based on sequence analysis, we believe that C17 has homology to IL-2 and hence we present the hypothesis that C17...

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Autores principales:	Connie Chao, Barbara Joyce-Shaikh, Jeff Grein, Mehrdad Moshrefi, Fahimeh Raoufi, Drake M Laface, Terril K McClanahan, Patricia A Bourne, Robert H Pierce, Daniel M Gorman, Stefan Pflanz
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/36a31a211e0b44ccbe73fcc7219c0ef5
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spelling	oai:doaj.org-article:36a31a211e0b44ccbe73fcc7219c0ef52021-11-18T06:49:31ZC17 prevents inflammatory arthritis and associated joint destruction in mice.1932-620310.1371/journal.pone.0022256https://doaj.org/article/36a31a211e0b44ccbe73fcc7219c0ef52011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21799806/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203C17 was first described about ten years ago as a gene expressed in CD34+ cells. A more recent study has suggested a role for C17 in chondrogenesis and development of cartilage. However, based on sequence analysis, we believe that C17 has homology to IL-2 and hence we present the hypothesis that C17 is a cytokine possessing immune-regulatory properties. We provide evidence that C17 is a secreted protein preferentially expressed in chondrocytes, hence in cartilage-rich tissues. Systemic expression of C17 in vivo reduces disease in a collagen antibody-induced arthritis model in mice (CAIA). Joint protection is evident by delayed disease onset, minimal edema, bone protection and absence of diverse histological features of disease. Expression of genes typically associated with acute joint inflammation and erosion of cartilage or bone is blunted in the presence of C17. Consistent with the observed reduction in bone erosion, we demonstrate reduced levels of RANKL in the paws and sera of mice over-expressing C17. Administration of C17 at the peak of disease, however, had no effect on disease progression, indicating that C17's immune-regulatory activity must be most prominent prior to or at the onset of severe joint inflammation. Based on this data we propose C17 as a cytokine that s contributes to immune homeostasis systemically or in a tissue-specific manner in the joint.Connie ChaoBarbara Joyce-ShaikhJeff GreinMehrdad MoshrefiFahimeh RaoufiDrake M LafaceTerril K McClanahanPatricia A BourneRobert H PierceDaniel M GormanStefan PflanzPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 7, p e22256 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Connie Chao Barbara Joyce-Shaikh Jeff Grein Mehrdad Moshrefi Fahimeh Raoufi Drake M Laface Terril K McClanahan Patricia A Bourne Robert H Pierce Daniel M Gorman Stefan Pflanz C17 prevents inflammatory arthritis and associated joint destruction in mice.
description	C17 was first described about ten years ago as a gene expressed in CD34+ cells. A more recent study has suggested a role for C17 in chondrogenesis and development of cartilage. However, based on sequence analysis, we believe that C17 has homology to IL-2 and hence we present the hypothesis that C17 is a cytokine possessing immune-regulatory properties. We provide evidence that C17 is a secreted protein preferentially expressed in chondrocytes, hence in cartilage-rich tissues. Systemic expression of C17 in vivo reduces disease in a collagen antibody-induced arthritis model in mice (CAIA). Joint protection is evident by delayed disease onset, minimal edema, bone protection and absence of diverse histological features of disease. Expression of genes typically associated with acute joint inflammation and erosion of cartilage or bone is blunted in the presence of C17. Consistent with the observed reduction in bone erosion, we demonstrate reduced levels of RANKL in the paws and sera of mice over-expressing C17. Administration of C17 at the peak of disease, however, had no effect on disease progression, indicating that C17's immune-regulatory activity must be most prominent prior to or at the onset of severe joint inflammation. Based on this data we propose C17 as a cytokine that s contributes to immune homeostasis systemically or in a tissue-specific manner in the joint.
format	article
author	Connie Chao Barbara Joyce-Shaikh Jeff Grein Mehrdad Moshrefi Fahimeh Raoufi Drake M Laface Terril K McClanahan Patricia A Bourne Robert H Pierce Daniel M Gorman Stefan Pflanz
author_facet	Connie Chao Barbara Joyce-Shaikh Jeff Grein Mehrdad Moshrefi Fahimeh Raoufi Drake M Laface Terril K McClanahan Patricia A Bourne Robert H Pierce Daniel M Gorman Stefan Pflanz
author_sort	Connie Chao
title	C17 prevents inflammatory arthritis and associated joint destruction in mice.
title_short	C17 prevents inflammatory arthritis and associated joint destruction in mice.
title_full	C17 prevents inflammatory arthritis and associated joint destruction in mice.
title_fullStr	C17 prevents inflammatory arthritis and associated joint destruction in mice.
title_full_unstemmed	C17 prevents inflammatory arthritis and associated joint destruction in mice.
title_sort	c17 prevents inflammatory arthritis and associated joint destruction in mice.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/36a31a211e0b44ccbe73fcc7219c0ef5
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C17 prevents inflammatory arthritis and associated joint destruction in mice.

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