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Dermal Melanocortin Receptor Rebound in Diffuse Systemic Sclerosis after Anti-TGF ss 1 Antibody Therapy
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
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2012 (engelsk)Inngår i: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 76, nr 5, s. 478-482Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Disturbed transforming growth factor beta (TGF beta) signalling leads to enhanced synthesis of extracellular matrix (ECM), which is manifested as systemic sclerosis (SSc), but this may be attenuated by the melanocortin system. Here, we report of rebound reaction in the gene expression of melanocortin receptor (MCR) subtypes and of the precursor of these receptors ligands, the pro-opio-melanocortin protein (POMC), in the acute skin lesion of diffuse systemic sclerosis (dSSc) after treatment with a recombinant human anti-TGF beta 1 antibody. Biopsies, taken from the leading edge of the skin lesion, before and after treatment of a patient with recent onset dSSc, were examined. Before treatment, increased levels of TGF beta mRNA and suppressed levels of POMC mRNA and MCR subtypes MC1-3, 5R mRNAs were seen in the lesion, compared with healthy controls. After treatment, there was a rebound expression of POMC, MC2, 3, 5R mRNAs. As the melanocortin system regulates collagen and melanin production, our findings add a new understanding to the pathogenetic mechanisms involved in the acute skin lesion of dSSc, which is characterized by enhanced ECM formation and changes in skin pigmentation.

sted, utgiver, år, opplag, sider
Hoboken: Wiley-Blackwell, 2012. Vol. 76, nr 5, s. 478-482
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Identifikatorer
URN: urn:nbn:se:umu:diva-61561DOI: 10.1111/j.1365-3083.2012.02757.xISI: 000309745900005OAI: oai:DiVA.org:umu-61561DiVA, id: diva2:572680
Tilgjengelig fra: 2012-11-28 Laget: 2012-11-20 Sist oppdatert: 2018-06-08bibliografisk kontrollert

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