Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/27538
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dc.contributor.authorBourke P.en
dc.contributor.authorBossingham D.en
dc.contributor.authorMackay F.en
dc.contributor.authorMorand E.F.en
dc.contributor.authorVincent F.B.en
dc.date.accessioned2021-05-14T09:16:20Zen
dc.date.available2021-05-14T09:16:20Zen
dc.date.copyright2013en
dc.date.created20130319en
dc.date.issued2013-03-19en
dc.identifier.citationInternal Medicine Journal. 43 (3) (pp 227-234), 2013. Date of Publication: March 2013.en
dc.identifier.issn1444-0903en
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/27538en
dc.description.abstractThe incidence and prevalence of autoimmune diseases such as rheumatoid arthritis, primary Sjogren syndrome, scleroderma and systemic lupus erythematosus (SLE) varies with geography and ethnicity. For example, SLE is reported to be more common in populations such as African-Caribbeans and Indigenous Australians (IA). As well as socio-economic status, variation in severity of disease may also show ethnic variability. The initial presentation of SLE in IA, in the context of a unique genetic background and distinctive environmental influences, is often florid with a recurring spectrum of clinical phenotypes. These clinical observations suggest a unique pathway for autoimmunity pathogenesis in this population. For instance, the high prevalence of bacterial infections in IA, particularly group A streptococcus, may be a potential explanation not only for increased incidence and prevalence of SLE but also the commonly florid acute disease presentation and propensity for rapidly progressive end organ threatening disease. This article will review the state of research in autoimmune disease of IA, consider key findings related to autoimmune disease in this population and propose a model potentially to explain the involvement of innate immunity and chronic infection in autoimmune disease pathogenesis. Ultimately, understanding of SLE at this level could affect management and result in personalised and targeted therapies to improve the health status of IA as well as better understanding of SLE pathogenesis per se. © 2012 Royal Australasian College of Physicians.en
dc.languageEnglishen
dc.languageenen
dc.publisherBlackwell Publishing (550 Swanston Street, Carlton South VIC 3053, Australia)en
dc.titleFocus on systemic lupus erythematosus in Indigenous Australians: Towards a better understanding of autoimmune diseases.en
dc.typeReviewen
dc.type.studyortrialReview article (e.g. literature review, narrative review)-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1111/imj.12039en
dc.publisher.placeAustraliaen
dc.identifier.pubmedid23176380 [http://www.ncbi.nlm.nih.gov/pubmed/?term=23176380]en
dc.identifier.source368419352en
dc.identifier.institution(Vincent, Mackay) Department of Immunology, Monash University, Central Clinical School, Alfred Medical Research and Education Precinct (AMREP), Australia (Morand) Centre for Inflammatory Diseases, Southern Clinical School, Monash University, Monash Medical Centre, Melbourne, VIC, Australia (Bourke) Division of Medicine, Royal Darwin Hospital, Department of Health, Tiwi, NT, Australia (Bossingham) Rheumatology Department, James Cook University, Cairns Base Hospital, Cairns, QLD, Australiaen
dc.description.addressF.B. Vincent, B lymphocyte, BAFF and Autoimmunity Laboratory, Department of Immunology, Monash University, Level 2, AMREP Building, 89 Commercial Road, Melbourne, VIC 3004, Australia. E-mail: vincent.fabien@gmail.comen
dc.description.publicationstatusEmbaseen
dc.rights.statementCopyright 2014 Elsevier B.V., All rights reserved.en
dc.subect.keywordsAutoimmunity B cell B cell activating factor of the tumour necrosis factor (TNF) family (BAFF) Indigenous Australian Innate immunity Systemic lupus erythematosus (SLE)en
dc.identifier.authoremailVincent F.B.; vincent.fabien@gmail.comen
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.openairetypeReview-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptRheumatology-
crisitem.author.deptCentre for Inflammatory Diseases at Monash Health-
crisitem.author.deptRheumatology-
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