Developing connections amongst key cytokines and dysregulated germinal centers in autoimmunity

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dc.contributor.authorSweet, Rebecca A
dc.contributor.authorLee, Sau K
dc.contributor.authorVinuesa, Carola
dc.date.accessioned2014-02-19T23:06:01Z
dc.date.available2014-02-19T23:06:01Z
dc.date.issued2012-11-01
dc.date.updated2015-12-08T08:39:06Z
dc.description.abstractSystemic autoimmunity owing to overactivity of Tfh and dysregulated germinal centers has been described in mice and humans. Cytokines such as IL-21, IFN-γ, IL-6 and IL-17 are elevated in the plasma of mouse models of lupus, arthritis, and multiple sclerosis, and in subsets of patients with autoimmune disease. Monoclonal antibodies targeting these cytokines are entering clinical trials. While these cytokines exert pleiotropic effects on immune cells and organs, it is becoming clear that each and all of them can profoundly regulate Tfh numbers and/or function and induce or maintain the aberrant germinal center reactions that lead to pathogenic autoantibody formation. Here we review recent discoveries into the roles of IL-21, IFN-γ, IL-6, and IL-17 in germinal center responses and antibody-driven autoimmunity. These new insights used in conjunction with biomarkers of an overactive Tfh pathway may help stratify patients to rationalize the use of emerging monoclonal anti-cytokine antibody therapies.
dc.description.sponsorshipR.A.S. is a Sir Keith Murdoch Fellow of the American Australian Association. C.G.V. is supported by an Elizabeth Blackburn NHMRC Fellowship. The Vinuesa Lab is supported by NHMRC program and project grants.en_AU
dc.format7 pages
dc.identifier.issn0952-7915
dc.identifier.urihttp://hdl.handle.net/1885/11397
dc.publisherElsevier
dc.rightshttp://www.sherpa.ac.uk/romeo/issn/0952-7915/author can archive pre-print (ie pre-refereeing) Sherpa/Romeo as at 20/2/14)
dc.sourceCurrent Opinion in Immunology 24.6 (2012): 658–664
dc.subjectsystemic autoimmunity
dc.subjectTfh
dc.subjectCytokines
dc.subjectpathogenic autoantibody formation
dc.titleDeveloping connections amongst key cytokines and dysregulated germinal centers in autoimmunity
dc.typeJournal article
local.bibliographicCitation.lastpage664
local.bibliographicCitation.startpage658
local.contributor.affiliationSweet, Rebecca A, Department of Pathogens and Immunity, John Curtin School of Medical Research, The Australian National University
local.contributor.affiliationLee, Sau K, Department of Pathogens and Immunity, John Curtin School of Medical Research, The Australian National University
local.contributor.affiliationVinuesa, Carola G, Department of Pathogens and Immunity, John Curtin School of Medical Research, The Australian National University
local.contributor.authoremailcarola.vinuesa@anu.edu.auen_AU
local.contributor.authoruidu4164556en_AU
local.identifier.absfor110703 - Autoimmunity
local.identifier.absfor110704 - Cellular Immunology
local.identifier.absfor110705 - Humoural Immunology and Immunochemistry
local.identifier.absseo920108 - Immune System and Allergy
local.identifier.absseo920116 - Skeletal System and Disorders (incl. Arthritis)
local.identifier.ariespublicationu9505948xPUB90
local.identifier.citationvolume24
local.identifier.doi10.1016/j.coi.2012.10.003
local.identifier.scopusID2-s2.0-84869870503
local.identifier.thomsonID000312359600003
local.identifier.uidSubmittedByu9505948en_AU
local.publisher.urlhttp://www.elsevier.com/en_AU
local.type.statusPublished Versionen_AU

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