About: Impact of Host Genetics and Biological Response Modifiers on Respiratory Tract Infections

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About: Impact of Host Genetics and Biological Response Modifiers on Respiratory Tract Infections Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Impact of Host Genetics and Biological Response Modifiers on Respiratory Tract Infections
Creator	Rodrigo, Carlos Blanco, Ignacio Domínguez, Jose Lacoma, Alicia Latorre, Irene Mateo, Lourdes Prat, Cristina Villar-Hernandez, Raquel Gonzalo-Asensio, Jesús Marriott, Ian Méndez, Maria Spaan, András
topic	covid:1df0f9012de37de02b7af4bd23931f626c7bbc71#this
source	Medline; PMC
abstract	Host susceptibility to respiratory tract infections (RTI) is dependent on both genetic and acquired risk factors. Repeated bacterial and viral RTI, such as pneumonia from encapsulated microorganisms, respiratory tract infections related to respiratory syncytial virus or influenza, and even the development of bronchiectasis and asthma, are often reported as the first symptom of primary immunodeficiencies. In the same way, neutropenia is a well-known risk factor for invasive aspergillosis, as well as lymphopenia for Pneumocystis, and mycobacterial infections. However, in the last decades a better knowledge of immune signaling networks and the introduction of next generation sequencing have increased the number and diversity of known inborn errors of immunity. On the other hand, the use of monoclonal antibodies targeting cytokines, such as tumor necrosis factor alpha has revealed new risk groups for infections, such as tuberculosis. The use of biological response modifiers has spread to almost all medical specialties, including inflammatory diseases and neoplasia, and are being used to target different signaling networks that may mirror some of the known immune deficiencies. From a clinical perspective, the individual contribution of genetics, and/or targeted treatments, to immune dysregulation is difficult to assess. The aim of this article is to review the known and newly described mechanisms of impaired immune signaling that predispose to RTI, including new insights into host genetics and the impact of biological response modifiers, and to summarize clinical recommendations regarding vaccines and prophylactic treatments in order to prevent infections.
has issue date	2019-05-07(xsd:dateTime)
bibo:doi	10.3389/fimmu.2019.01013
bibo:pmid	31134083
has license	cc-by
sha1sum (hex)	1df0f9012de37de02b7af4bd23931f626c7bbc71
schema:url	https://doi.org/10.3389/fimmu.2019.01013
resource representing a document's title	Impact of Host Genetics and Biological Response Modifiers on Respiratory Tract Infections
has PubMed Central identifier	PMC6513887
has PubMed identifier	31134083
schema:publication	Front Immunol
resource representing a document's body	covid:1df0f9012de37de02b7af4bd23931f626c7bbc71#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/1df0f9012de37de02b7af4bd23931f626c7bbc71
is schema:about of	named entity 'Infections' named entity 'Biological' named entity 'MINI' named entity 'REVIEW' named entity 'IMPACT' named entity 'MINI' named entity 'GENETICS' named entity 'RESPIRATORY TRACT INFECTIONS' named entity 'HOST' named entity 'BIOLOGICAL RESPONSE MODIFIERS' named entity 'Genetics' named entity 'disease control' named entity 'monogenic' named entity 'pulmonary infections' named entity 'immune responses' named entity 'organizing pneumonia' named entity 'IgG2' named entity 'life-threatening' named entity 'pleiotropic' named entity 'TNF-α' named entity 'rheumatologic' named entity 'M. tuberculosis' named entity 'susceptibility to disease' named entity 'non-tuberculous mycobacteria' named entity 'Biological therapies' named entity 'PATHOGENESIS' named entity 'general population' named entity 'genetic defects' named entity 'pneumonia' named entity 'exome' named entity 'receptor' named entity 'immune deficiencies' named entity 'BRM' named entity 'IFN-γ' named entity 'humoral responses' named entity 'inborn errors' named entity 'infection' named entity 'asthma' named entity 'genetic studies' named entity 'biological therapy' named entity 'innate immunity' named entity 'tuberculin skin test' named entity 'Miguel Servet' named entity 'etanercept' named entity 'commensalism' named entity 'TLR' named entity 'corticosteroid' named entity 'infectious diseases' named entity 'RTI' named entity 'WGAS' named entity 'invitro' named entity 'immune-mediated' named entity 'bacterial pneumonia' named entity 'vaccines' named entity 'IL-1' named entity 'mycobacterial' named entity 'NOD-like receptors' named entity 'lung' named entity 'psoriatic arthritis' named entity 'genetic susceptibility' named entity 'congenital defects' named entity 'BRM' named entity 'interleukin' named entity 'mucociliary clearance' named entity 'targeted treatments' named entity 'anergy' named entity 'PRR' named entity 'immunomodulation'

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