dc.contributorhttps://orcid.org/0000-0002-3403-9849
dc.creatorPacheco Tovar, Deyanira del Carmen
dc.creatorLópez Luna, Argelia
dc.creatorHerrera Esparza, Rafael
dc.creatorAvalos Díaz, Esperanza del Refugio
dc.date.accessioned2020-12-09T18:58:54Z
dc.date.available2020-12-09T18:58:54Z
dc.date.created2020-12-09T18:58:54Z
dc.date.issued2011-01-03
dc.identifier2090-6552
dc.identifier2090-6544
dc.identifier2090-6552
dc.identifierhttp://ricaxcan.uaz.edu.mx/jspui/handle/20.500.11845/2186
dc.identifierhttps://doi.org/10.48779/3rer-2628
dc.description.abstractApoptosis 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.languageeng
dc.publisherHindawi
dc.relationPROMPEP
dc.relationgeneralPublic
dc.relationhttps://www.hindawi.com/journals/ad/2011/563091/
dc.sourceAutoimmune Diseases Vol. 2011, pp. 1-9
dc.titleThe Caspase Pathway as a Possible Therapeutic Target in Experimental Pemphigus
dc.typeinfo:eu-repo/semantics/article


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