dc.contributor | https://orcid.org/0000-0002-3403-9849 | |
dc.creator | Pacheco Tovar, Deyanira del Carmen | |
dc.creator | López Luna, Argelia | |
dc.creator | Herrera Esparza, Rafael | |
dc.creator | Avalos Díaz, Esperanza del Refugio | |
dc.date.accessioned | 2020-12-09T18:58:54Z | |
dc.date.available | 2020-12-09T18:58:54Z | |
dc.date.created | 2020-12-09T18:58:54Z | |
dc.date.issued | 2011-01-03 | |
dc.identifier | 2090-6552 | |
dc.identifier | 2090-6544 | |
dc.identifier | 2090-6552 | |
dc.identifier | http://ricaxcan.uaz.edu.mx/jspui/handle/20.500.11845/2186 | |
dc.identifier | https://doi.org/10.48779/3rer-2628 | |
dc.description.abstract | Apoptosis plays a roles in phemphigus IgG-dependent acantholysis; theoretically, the blockade of the caspase pathway could prevent the blistering that is caused by pemphigus autoantibodies. Using this strategy, we attempted to block the pathogenic effect ofpemphigus IgG in Balb/c mice by using the caspase inhibitor Ac-DEVD-CMK. This inhibitor was administrated before theinjection of pemphigus IgG into neonatal mice. The main resultsof the present investigation are as follows: pemphigusIgG induces intraepidermal blisters in Balb/c neonatal mice; keratinocytes around the blister and acantholytic cells undergoapoptosis; the caspases inhibitor Ac-DEVD-CMK prevents apoptosis; the inhibition of the caspase pathway prevents blisterformation. In conclusion, inhibition of the caspase pathway may be a promising therapeutic tool that can help in the treatment ofpemphigus flare ups. | |
dc.language | eng | |
dc.publisher | Hindawi | |
dc.relation | PROMPEP | |
dc.relation | generalPublic | |
dc.relation | https://www.hindawi.com/journals/ad/2011/563091/ | |
dc.source | Autoimmune Diseases Vol. 2011, pp. 1-9 | |
dc.title | The Caspase Pathway as a Possible Therapeutic Target in Experimental Pemphigus | |
dc.type | info:eu-repo/semantics/article | |