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Titolo:
Major histocompatibility complex and tumor necrosis factor-alpha polymorphisms in pigeon breeder's disease
Autore:
Camarena, A; Juarez, A; Mejia, M; Estrada, A; Carrillo, G; Falfan, R; Zuniga, J; Navarro, C; Granados, J; Selman, M;
Indirizzi:
Inst Nacl Enfermedades Resp, Mexico City 14080, DF, Mexico Inst Nacl Enfermedades Resp Mexico City DF Mexico 14080 14080, DF, Mexico Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Mexico City, DF, Mexico Inst Nacl Ciencias Med & Nutr Salvador Zubiran Mexico City DF Mexico ico
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
fascicolo: 7, volume: 163, anno: 2001,
pagine: 1528 - 1533
SICI:
1073-449X(200106)163:7<1528:MHCATN>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYSTEMIC LUPUS-ERYTHEMATOSUS; EXTRINSIC ALLERGIC ALVEOLITIS; HYPERSENSITIVITY PNEUMONITIS; BRONCHOALVEOLAR LAVAGE; PROMOTER REGION; HLA-DQ; LUNG; ASSOCIATION; RELEVANCE; DIAGNOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Selman, M Inst Nacl Enfermedades Resp, Tlalpan 4502,Col Secc 16, Mexico City 14080, DF, Mexico Inst Nacl Enfermedades Resp Tlalpan 4502,Col Secc 16 Mexico City DF Mexico 14080
Citazione:
A. Camarena et al., "Major histocompatibility complex and tumor necrosis factor-alpha polymorphisms in pigeon breeder's disease", AM J R CRIT, 163(7), 2001, pp. 1528-1533

Abstract

Pigeon breeders disease (PBD) is caused by the exposure of a susceptible host to avian antigens. However, genetic factors determining individual predisposition are unknown. In this work, polymorphisms of the major histocompatibility complex (MHC) class II alleles end tumor necrosis factor alpha (TNF-alpha) promoter were evaluated in 44 patients with PBD, 99 healthy unrelated controls (HC), and 50 exposed but asymptomatic subjects (EAS). MHC typing was performed by PCR-specific sequence oligonucleotide analysis, and TNF-alpha polymorphism at -238 and -308 positions by amplification refractory mutation system-PCR. PBD patients showed a significant increase of the alleles HLA-DRB1*1305 (p < 0.001, OR = 15.4, 95%: CI = 3.18-102.6 [HC], and OR = 17.05, 95% Cl = 2.25-357.8 [EAS]) and HLA-DQB1*0501 (p < 0.05, OR = 2.93,95% CI = 1.21-7.15 [HC], and OR = 2.96, 95% CL = 1.0-9.14 [EAS]). A decrease of HLA-DRB1*0802 was also noticed in patients when compared: with both control groups (p < 0.05). Haplotype analysis revealed an increase of DRB1*1305-DQB1*0301 and a decrease of DRB1*0802-DQB1*0402. PBD patients had an increased frequency of TNF-2(-308) compared with both control groups (p < 0.05). Patients exhibiting the TNF-2(-308) allele were younger (33.9 +/- 14.6 versus 44.2 +/- 70.4 yr; p < 0.05), and displayed more lymphocytes in theirbronchoalveolar lavages (88.0 +/- 12.1 versus 68.9 +/- 17.2; p < 0.05). These results suggest that genetic factors located within the MHC region contribute to the development of PBD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 08:36:00