Analysis of Il-10 gene sequence in patients with sinonasal polyposis

Sinonasal polyposis (SNP) is a chronic inflammatory disease of nasal and paranasal cavities. Human leukocyte antigen-G molecules (HLA-G) are non-classic HLA-I molecules with anti-inflammatory and tolerogenic properties. HLA-G production is mainly induced by interleukin (IL)-10. IL-10 is an anti-infl...

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Bibliographic Details
Published in:International journal of immunopathology and pharmacology 2015-09, Vol.28 (3), p.434-439
Main Authors: Malagutti, N, Stomeo, F, Pelucchi, S, Ronchin, R, Ceccon, M, Malacrida, G, Ciorba, A, Pastore, A, Borin, M, Rizzo, R
Format: Article
Language:English
Subjects:
Adult
Cytokines - genetics
Female
Histocompatibility Antigens Class I - genetics
HLA-G Antigens - genetics
Humans
Interleukin-10 - genetics
Lipopolysaccharide Receptors - genetics
Male
Monocytes - metabolism
Nasal Polyps - genetics
Receptors, Interleukin-10 - genetics
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Summary:Sinonasal polyposis (SNP) is a chronic inflammatory disease of nasal and paranasal cavities. Human leukocyte antigen-G molecules (HLA-G) are non-classic HLA-I molecules with anti-inflammatory and tolerogenic properties. HLA-G production is mainly induced by interleukin (IL)-10. IL-10 is an anti-inflammatory cytokine that inhibits the production of proinflammatory cytokines and induces HLA-class II down-modulation. Recent studies suggest that HLA-G could play a role in SNP pathogenesis; in SNP patients physiological levels of IL-10 (produced by activated peripheral blood CD14+ monocytes) are not able to induce production of HLA-G. Different mechanisms could justify these findings: genomic or amino-acidic sequence alterations in IL-10 lower IL-10 receptor expression, lower IL-10 receptor affinity, or alterations of the intracellular signal transmission. This study analyzes nucleotidic sequence of IL-10 gene in SNP patients. Sequencing of IL-10 gene shows that the lack of HLA-G production by peripheral blood CD14+ monocytes is not related to alterations in IL-10 gene nucleotidic sequence.
ISSN:0394-6320
2058-7384
DOI:10.1177/0394632015573922