A certain class of antibiotics prompts cells to produce low levels of novel self proteins that could trigger an autoimmune disease, research suggests.
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Nuria Parra Macías's curator insight,
February 8, 2014 3:24 AM
Inmunomedia 3.0: una pica en Flandes en innovación docente. El ejemplo de flipped classroom de la facultad de Medicina de la universidad de Valladolid.
Alfredo Corell's comment,
February 12, 2014 3:20 PM
Cualquier tipo de difusión entre personal docente afin es bienvenida, así que gracias de corazón!!1
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Alfredo Corell's curator insight,
April 23, 2013 2:14 PM
By Mobeen Syed part 1: http://www.youtube.com/watch?v=GKf8-Ex6F7Y&list=TLv1_K8sf8xWw part 2: http://www.youtube.com/watch?v=j7vlkt93UEc&list=TLv1_K8sf8xWw Part 3: http://www.youtube.com/watch?v=wap9Ilm7HPE&list=TLv1_K8sf8xWw part 4: http://www.youtube.com/watch?v=u5O2avcbkzY&list=TLv1_K8sf8xWw part 5: http://www.youtube.com/watch?v=PLCPjFsD8Kc&list=TLv1_K8sf8xWw
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Link to the PNAS journal: http://www.pnas.org/content/early/2014/03/26/1402670111
SignificanceMany genetic disorders, including Duchenne muscular dystrophy and cystic fibrosis, are caused by a defective protein resulting from a premature termination codon (PTC) in the mutant gene. Aminoglycosides have been proposed as therapies for these disorders because they increase the frequency of translational read-through of PTCs, permitting expression of full-length protein. We consider the possibility that this approach may prompt an autoimmune response to HLA-presented epitopes encoded downstream of the PTC or other stop codons. We demonstrate that gentamicin induces immunologically relevant levels of an epitope derived from PTC read-through. Furthermore, we identify multiple HLA class I-binding peptides derived from read-through of conventional stop codons in gentamicin-treated cells. These results substantiate the possibility of immune autoreactivity from read-through therapies.