Cited by 81Antifungal resistance and susceptibilityImmunodeficiency and Autoimmune DisordersFungal and yeast genetics research

Variable number of tandem repeats of TNF receptor type 2 promoter as genetic biomarker of susceptibility to develop invasive pulmonary aspergillosis

Sainz, Juan, Pérez, Eva, Hassan, Laila, Moratalla, Antonio, Romero, Antonio, Collado, María Dolores, Jurado, Manuel·2007·Human Immunology

Abstract

Tumor necrosis factor alpha (TNF-alpha) and lymphotoxin alpha (LT-alpha) are pivotal mediators of inflammatory responses in fungal infection diseases. We hypothesized that polymorphisms in genes of these cytokines or their receptors might increase the susceptibility of hematologic patients to develop invasive pulmonary aspergillosis (IPA). One hundred two hematologic patients and 124 age-matched controls were enrolled in the study, and the following standard single nucleotide polymorphisms were investigated: TNF-alpha -308 and +489, LT-alpha +252 and Tumor Necrosis Factor Receptor 2 (TNFR2) +676. Variable number of tandem repeats (VNTRs) at position -322 of the TNFR2 gene were also studied. Genotypic and allelic frequencies were similar between patients and controls. IPA was diagnosed in 54 of the 102 patients according to consensus criteria published by the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group. TNF-alpha and LT-alpha polymorphisms were not associated with presence of IPA. Susceptibility to IPA was strongly associated with VNTR at position -322 in the promoter region of the TNR2 gene (p = 0.029) but was not associated with the presence of TNFR2 +676 polymorphism. A genetic difference in TNFR2 promoter VNTR may play a major role in susceptibility to IPA infection.

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Crossref · 10.1016/j.humimm.2006.10.011

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  • Polymorphisms within the tumor necrosis factor-alpha gene and its receptors are associated with susceptibility to aspergillosis.

    “Polymorphisms within the tumor necrosis factor-α (TNF-α) gene [32] and its receptors [37,38] have also been associated with susceptibility to aspergillosis.”

    From Race and ethnicity: Risk factors for fungal infections? (2023) · cites this paper as [38]

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Authors
Sainz, J., Pérez, E., Hassan, L., Moratalla, A., Romero, A., Collado, M. D., & Jurado, M.
Affiliations
Hospital Universitario Virgen de las Nieves (ES)
Venue
Human Immunology
Publisher
Elsevier BV
Published
2007-01
Volume
68
Issue
1
Pages
41-50
ISSN
0198-8859 (ISSN-L)
OpenAlex
W2053563213
Cited by
81
References
62
Citations by year
2024: 2 · 2023: 2 · 2022: 2 · 2021: 5 · 2020: 5 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 6 · 2015: 5 · 2014: 4 · 2013: 2 · 2012: 4
FWCI
3.49
Type
journal article
Language
en
Open access
closed
Locations
  • Human Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Servicio Andaluz de Salud (1/02/06)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Keywords
invasive pulmonary aspergillosis, variable number tandem repeats, promoter polymorphism, genetic susceptibility, hematologic patients, TNF-α, lymphotoxin, single nucleotide polymorphisms, fungal infection susceptibility, genetic biomarkers
MeSH terms
Aspergillosis, Female, Genetic Markers, Humans, Lung Diseases, Fungal, Male, Middle Aged, Promoter Regions, Genetic, Prospective Studies, Minisatellite Repeats, Genetic Predisposition to Disease, Receptors, Tumor Necrosis Factor, Type II

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