“…The authors concluded that the major therapeutic effect of CH was due to reduction of antibody synthesis rather than modification of the events that occur within the epidermis after antibody binding. In turn, the adequacy of the conclusion drawn from the in vivo experiment has been challenged by the well established clinical fact that pulse therapy with a high dose of an intravenous administered glucocorticosteroid agent, such as MP, can stop acantholysis in PV patients within 24 -48 h, which is too early to induce changes in the serum titer of pemphigus autoantibodies (22,25,26). Therefore, we hypothesized that the discrepancy among the results of in vitro and in vivo experiments reported previously might be due to limitations of the mouse model used by Anhalt et al (3,84), and we sought to develop an adequate model for in vivo testing the anti-acantholytic efficacy of CH in pemphigus.…”