The study of interactions between genome and exposome in the development of systemic lupus erythematosus. [Review]

MedStar author(s):
Citation: Autoimmunity Reviews. 18(4):382-392, 2019 Apr.PMID: 30772495Institution: MedStar Washington Hospital CenterDepartment: Medicine/RheumatologyForm of publication: Journal ArticleMedline article type(s): Journal Article | ReviewSubject headings: *Environmental Exposure/ae [Adverse Effects] | *Gene-Environment Interaction | *Lupus Erythematosus, Systemic/ge [Genetics] | Case-Control Studies | Genetic Predisposition to Disease | Genome, Human/ph [Physiology] | Genotype | Humans | Lupus Erythematosus, Systemic/ep [Epidemiology] | Lupus Erythematosus, Systemic/et [Etiology] | Lupus Erythematosus, Systemic/pa [Pathology]Year: 2019ISSN:
  • 1568-9972
Name of journal: Autoimmunity reviewsAbstract: Copyright (c) 2019 The Author(s). Published by Elsevier B.V. All rights reserved.Systemic lupus erythematosus (SLE) is a systemic inflammatory autoimmune disease characterized by a broad spectrum of clinical and serological manifestations. This may reflect a complex and multifactorial etiology involving several identified genetic and environmental factors, though not explaining the full risk of SLE. Established SLE risk genotypes are either very rare or with modest effect sizes and twin studies indicate that other factors besides genetics must be operative in SLE etiology. The exposome comprises the cumulative environmental influences on an individual and associated biological responses through the lifespan. It has been demonstrated that exposure to silica, smoking and exogenous hormones candidate as environmental risk factors in SLE, while alcohol consumption seems to be protective. Very few studies have investigated potential gene-environment interactions to determine if some of the unexplained SLE risk is attributable hereto. Even less have focused on interactions between specific risk genotypes and environmental exposures relevant to SLE pathogenesis. Cohort and case-control studies may provide data to suggest such biological interactions and various statistical measures of interaction can indicate the magnitude of such. However, such studies do often have very large sample-size requirements and we suggest that the rarity of SLE to some extent can be compensated by increasing the ratio of controls. This review summarizes the current body of knowledge on gene-environment interactions in SLE. We argue for the prioritization of studies that comprise the increasing details available of the genome and exposome relevant to SLE as they have the potential to disclose new aspects of SLE pathogenesis including phenotype heterogeneity.All authors: Collins C, Jacobsen S, Lange T, Leffers HCB, Ulff-Moller CJFiscal year: FY2019Digital Object Identifier: Date added to catalog: 2019-03-14
Holdings
Item type Current library Collection Call number Status Date due Barcode
Journal Article MedStar Authors Catalog Article 30772495 Available 30772495

Copyright (c) 2019 The Author(s). Published by Elsevier B.V. All rights reserved.

Systemic lupus erythematosus (SLE) is a systemic inflammatory autoimmune disease characterized by a broad spectrum of clinical and serological manifestations. This may reflect a complex and multifactorial etiology involving several identified genetic and environmental factors, though not explaining the full risk of SLE. Established SLE risk genotypes are either very rare or with modest effect sizes and twin studies indicate that other factors besides genetics must be operative in SLE etiology. The exposome comprises the cumulative environmental influences on an individual and associated biological responses through the lifespan. It has been demonstrated that exposure to silica, smoking and exogenous hormones candidate as environmental risk factors in SLE, while alcohol consumption seems to be protective. Very few studies have investigated potential gene-environment interactions to determine if some of the unexplained SLE risk is attributable hereto. Even less have focused on interactions between specific risk genotypes and environmental exposures relevant to SLE pathogenesis. Cohort and case-control studies may provide data to suggest such biological interactions and various statistical measures of interaction can indicate the magnitude of such. However, such studies do often have very large sample-size requirements and we suggest that the rarity of SLE to some extent can be compensated by increasing the ratio of controls. This review summarizes the current body of knowledge on gene-environment interactions in SLE. We argue for the prioritization of studies that comprise the increasing details available of the genome and exposome relevant to SLE as they have the potential to disclose new aspects of SLE pathogenesis including phenotype heterogeneity.

English

Powered by Koha