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001-es BibID:	BIBFORM065561
Első szerző:	Bácsi Attila (immunológus)
Cím:	Pathophysiology of bronchoconstriction : role of Oxidatively Damaged DNA Repair / Attila Bacsi, Lang Pan, Xueqing Ba, Istvan Boldogh
Dátum:	2016
ISSN:	1528-4050 1473-6322
Megjegyzések:	PURPOSE OF REVIEW:To provide an overview on the present understanding of roles of oxidative DNA damage repair in cell signaling underlying bronchoconstriction common to, but not restricted to various forms of asthma and chronic obstructive pulmonary disease.RECENT FINDINGS:Bronchoconstriction is a tightening of smooth muscle surrounding the bronchi and bronchioles with consequent wheezing and shortness of breath. Key stimuli include air pollutants, viral infections, allergens, thermal and osmotic changes, and shear stress of mucosal epithelium, triggering a wide range of cellular, vascular, and neural events. Although activation of nerve fibers, the role of G-proteins, protein kinases and Ca++, and molecular interaction within contracting filaments of muscle are well defined, the overarching mechanisms by which a wide range of stimuli initiate these events are not fully understood. Many, if not all, stimuli increase levels of reactive oxygen species, which are signaling and oxidatively modifying macromolecules, including DNA. The primary reactive oxygen species target in DNA is guanine, and 8-oxoguanine is one of the most abundant base lesions. It is repaired by 8-oxoguanine DNA glycosylase1 during base excision repair processes. The product, free 8-oxo-7,8-dihydro-2'-deoxyguanosine base, is bound by 8-oxoguanine DNA glycosylase1 with high affinity, and the complex then functions as an activator of small guanosine triphosphatases, triggering pathways for inducing gene expression and contraction of intracellular filaments in mast and smooth muscle cells.SUMMARY:Oxidative DNA damage repair-mediated cell activation signaling result in gene expression that 'primes' the mucosal epithelium and submucosal tissues to generate mediators of airway smooth muscle contractions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban muscle constriction oxidative DNA damage 8-oxoguanine DNA glycosylase1 small GTPases
Megjelenés:	Current Opinion In Allergy And Clinical Immunology 16 : 1 (2016), p. 59-67. -
További szerzők:	Pan, Lang Ba, Xueqing Boldogh István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM041846
035-os BibID:	PMID:23026768
Első szerző:	Puel, Anne
Cím:	Inborn errors of human IL-17 immunity underlie chronic mucocutaneous candidiasis / Anne Puel, Sophie Cypowyj, László Maródi, Laurent Abel, Capucine Picard, Jean-Laurent Casanova
Dátum:	2012
Megjegyzések:	Chronic mucocutaneous candidiasis (CMC) is characterized by recurrent or persistent symptomatic infection of the nails, skin and mucosae mostly by Candida albicans. CMC is common in patients with profound primary T-cell immunodeficiency, who often display multiple infectious and autoimmune diseases. Patients with syndromic CMC, including autosomal dominant hyper IgE syndrome (AD-HIES) and autosomal recessive autoimmune polyendocrinopathy syndrome type I (APS-I), display fewer other infections. Patients with isolated CMC (CMCD) rarely display any other severe disease. We review here recent progress in the genetic dissection of these three types of inherited CMC. RECENT FINDINGS: Low IL-17 T-cell proportions were reported in patients with AD-HIES bearing heterozygous STAT3 mutations, prone to CMC and staphylococcal diseases, and in a kindred with autosomal recessive CARD9 deficiency, prone to CMC and other fungal infections. High levels of neutralizing autoantibodies against IL-17 cytokines were documented in patients with APS-I presenting with CMC as their only infectious disease. The first three genetic causes of CMCD were then reported: autosomal recessive IL-17RA and autosomal dominant IL-17F deficiencies and autosomal dominant STAT1 gain-of-function, impairing IL-17-producing T-cell development. SUMMARY: Inborn errors of human IL-17 immunity underlie CMC. Impaired IL-17 immunity may therefore account for CMC in other settings, including patients with acquired immunodeficiency.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény hazai lapban külföldön készült közlemény
Megjelenés:	Current Opinion in Allergy and Clinical Immunology. - 12 : 6 (2012), p. 616-622. -
További szerzők:	Cypowyj, Sophie Abel, Laurent Picard, Capucine Casanova, Jean-Laurent Maródi László (1949-) (gyermekgyógyász infektológus, immunológus)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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