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dc.creatorLlanos,Carolina
dc.creatorCarreño,Leandro J
dc.creatorKalergis,Alexis M
dc.date2011-01-01
dc.date.accessioned2019-05-02T21:21:59Z
dc.date.available2019-05-02T21:21:59Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602011000100007
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/82110
dc.descriptionUnder healthy conditions, there is a balance between tolerance to self-tissue constituents and immunity against foreign antigens. Autoimmunity diseases (AD) take place when that equilibrium is disrupted and the immune response is directed to self-antigens, leading to injury or destruction of host tissues. The mechanisms conducing to the loss of immune tolerance remain largely unknown. The recent appearance of biological therapies has contributed to significant reduction in morbidity. However, currently available therapies are associated with important side effects and work only as palliative treatments. Dendritic cells (DCs) have emerged as key players in developing and maintaining adaptive immunity due to their capacity to prime and modulate T cell function. Therefore, because DCs work as central modulators of immune tolerance, it is likely that alterations in their function can lead to the onset of autoimmune-inflammatory diseases. By modulating DC function, novel pathways in antigen-specific tolerance could be established. In this article, the possible contribution of altered DC-T cell interactions to the onset of autoimmunity are discussed. In addition, we expand on the notion that some of the functions of these cells could be relevant targets for intervening therapies aimed to restore the balance or even prevent the loss of tolerance.
dc.formattext/html
dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602011000100007
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.44 n.1 2011
dc.subjectdendritic cells
dc.subjectT cells
dc.subjectimmunological synapse
dc.subjectautoimmunity
dc.subjecttolerance
dc.titleContribution of dendritic cell/T cell interactions to triggering and maintaining autoimmunity


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