Macrophage Migration Inhibitory Factor (MIF) and Its Homologue D-Dopachrome Tautomerase (DDT) Inversely Correlate with Inflammation in Discoid Lupus Erythematosus

Bibliographic Details
Title: Macrophage Migration Inhibitory Factor (MIF) and Its Homologue D-Dopachrome Tautomerase (DDT) Inversely Correlate with Inflammation in Discoid Lupus Erythematosus
Authors: Rosario Caltabiano, Rocco De Pasquale, Eliana Piombino, Giorgia Campo, Ferdinando Nicoletti, Eugenio Cavalli, Katia Mangano, Paolo Fagone
Source: Molecules, Vol 26, Iss 1, p 184 (2021)
Publisher Information: MDPI AG, 2021.
Publication Year: 2021
Collection: LCC:Organic chemistry
Subject Terms: discoid lupus erythematosus, macrophage migration inhibitory factor, d-dopachrome tautomerase, Organic chemistry, QD241-441
More Details: Discoid Lupus Erythematosus (DLE) is a chronic cutaneous disease of unknown etiology and of immunoinflammatory origin that is characterized by inflammatory plaques and may lead to disfiguring scarring and skin atrophy. Current treatments are limited, with a large proportion of patients either poorly or not responsive, which makes DLE an unmet medical need. Macrophage migration inhibitory factor (MIF) is the prototype of a pleiotropic family of cytokine that also includes the recently discovered homologue D-dopachrome tautomerase (DDT) or MIF2. MIF and DDT/MIF-2 exert several biological properties, primarily, but not exclusively of a proinflammatory nature. MIF and DDT have been suggested to play a key role in the pathogenesis of several autoimmune diseases, such as multiple sclerosis and type 1 diabetes, as well as in the development and progression of certain forms of cancers. In the present study, we have performed an immunohistochemistry analysis for the evaluation of MIF in DLE lesions and normal skin. We found high levels of MIF in the basal layer of the epidermis as well as in the cutaneous appendage (eccrine glands and sebocytes) of normal skin. In DLE lesions, we observed a significant negative correlation between the expression of MIF and the severity of inflammation. In addition, we performed an analysis of MIF and DDT expression levels in the skin of DLE patients in a publicly available microarray dataset. Interestingly, while these in silico data only evidenced a trend toward reduced levels of MIF, they demonstrated a significant pattern of expression and correlation of DDT with inflammatory infiltrates in DLE skins. Overall, our data support a protective role for endogenous MIF and possibly DDT in the regulation of homeostasis and inflammation in the skin and open up novel avenues for the treatment of DLE.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1420-3049
Relation: https://www.mdpi.com/1420-3049/26/1/184; https://doaj.org/toc/1420-3049
DOI: 10.3390/molecules26010184
Access URL: https://doaj.org/article/5ce7a533aeaf464b80f57e5f738068e0
Accession Number: edsdoj.5ce7a533aeaf464b80f57e5f738068e0
Database: Directory of Open Access Journals
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More Details
ISSN:14203049
DOI:10.3390/molecules26010184
Published in:Molecules
Language:English