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E-selectin and P-selectin expression in endothelium of leprosy skin lesions

[Display omitted] •Leprosy is a disease whose clinical spectrum depends on the cytokine patterns.•Different adhesins participate of the immune response in infectious disease.•Endothelium activation are fundamental for immunity in leprosy. Leprosy is an infectious–contagious disease whose clinical ev...

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Published in:Acta tropica 2015-09, Vol.149, p.227-231
Main Authors: Souza, Juarez de, Sousa, Jorge Rodrigues de, Hirai, Kelly Emi, Silva, Luciana Mota, Fuzii, Hellen Thais, Dias, Leonidas Braga, Carneiro, Francisca Regina Oliveira, Aarão, Tinara Leila de Souza, Quaresma, Juarez Antonio Simões
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Language:English
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Summary:[Display omitted] •Leprosy is a disease whose clinical spectrum depends on the cytokine patterns.•Different adhesins participate of the immune response in infectious disease.•Endothelium activation are fundamental for immunity in leprosy. Leprosy is an infectious–contagious disease whose clinical evolution depends on the immune response pattern of the host. Adhesion molecules and leukocyte migration from blood to tissue are of the utmost importance for the recognition and elimination of infectious pathogens. Selectins are transmembrane glycoproteins that share a similar structural organization and can be divided into three types according to their site of expression. The biopsies were cut into 5μm thick sections and submitted to immunohistochemistry using antibodies against E-selectin and P-selectin. The number of E-selectin-positive cells was significantly higher in the tuberculoid form than in the lepromatous form. The immunostaining pattern of P-selectin differed from that of E-selectin. Analysis showed a larger number of endothelial cells expressing CD62P in the lepromatous form compared to the tuberculoid form. The presence of these adhesins in the endothelium contributing to or impairing the recruitment of immune cells to inflamed tissue and consequently influences the pattern of immune response and the clinical presentation of the disease.
ISSN:0001-706X
1873-6254
DOI:10.1016/j.actatropica.2015.06.002