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Autoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3

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dc.creatorGómez Osorio L.M.spa
dc.creatorMartín Ibañez J.spa
dc.creatorAnaya, Juan-Manuelspa
dc.date.accessioned2020-05-26T00:11:36Z
dc.date.available2020-05-26T00:11:36Z
dc.date.created2005spa
dc.description.abstractCo-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of T-cells. An important cellular group implicated in the regulation of co-stimulation is known as regulatory T cells (Treg). These cells can be used clinically in treatments ranging from cellular transfer in transplant patients to autoimmune diseases and suppression in cancer patients. Treg act through CTLA-4 molecules, which have the ability to suppress the co-stimulation signals and to stop the T cell response. Recently, CTLA-4Ig fusion molecules have been developed, which can block the presentation of auto-antigens. FOXP3 transcription factor is a specific molecule present in Treg that inhibits the production of IL-2 by CD4+ activated cells. Currently, FOXP3 functions are being extensively studied in order to develop new therapeutic targets. This article reviews co-signaling and its mechanism in Treg (CTLA-4, FOXP3), as well as its role in the physiopathology of autoimmune diseases.eng
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/24315
dc.language.isoengspa
dc.relation.citationEndPage297
dc.relation.citationIssueNo. 3
dc.relation.citationStartPage283
dc.relation.citationTitleInmunologia
dc.relation.citationVolumeVol. 24
dc.relation.ispartofInmunologia, Vol.24, No.3 (2005); pp. 283-297spa
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-29444445787&partnerID=40&md5=1e4580a5c4146c14f1a849d44ab7c38dspa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordCytotoxic T lymphocyte antigen 4spa
dc.subject.keywordTranscription factor FOXP3spa
dc.subject.keywordAntigen presentationspa
dc.subject.keywordAutoimmunityspa
dc.subject.keywordCell differentiationspa
dc.subject.keywordCell functionspa
dc.subject.keywordCell stimulationspa
dc.subject.keywordGene repressionspa
dc.subject.keywordGenetic transcriptionspa
dc.subject.keywordHumanspa
dc.subject.keywordMolecular dynamicsspa
dc.subject.keywordNonhumanspa
dc.subject.keywordPromoter regionspa
dc.subject.keywordReviewspa
dc.subject.keywordSignal transductionspa
dc.subject.keywordT lymphocytespa
dc.subject.keywordAutoimmune Diabetesspa
dc.subject.keywordAutoimmunityspa
dc.subject.keywordCo-signalingspa
dc.subject.keywordCTLA-4spa
dc.subject.keywordFOXP3spa
dc.subject.keywordRegulatory T cellsspa
dc.subject.keywordRheumatoid Arthritisspa
dc.subject.keywordSystemic Lupus Erythematosusspa
dc.titleAutoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3spa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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