Both pimecrolimus and corticosteroids deplete plasmacytoid dendritic cells in patients with atopic dermatitis.

ELISA as well as immunoblotting, although serum was obtained only at day 6 (SSSS no. 6 in Table 2). No antiDsg3 IgG was detected either by ELISA or by immunoblotting in these patients studied throughout their course, indicating the specificity of the reactivity against Dsg1 (Table 1). No apparent IgM reactivity against Dsg1 or Dsg3 was detected by ELISA (data not shown). None of the 12 patients with BI, whose sera were taken with a range of days 2–33, showed any detectable IgG production against either Dsg1 or Dsg3 as determined by ELISA and immunoblotting (Table 1). These findings indicate that a small number of patients of SSSS develop low titers of IgG antibodies specific for Dsg1 after binding and systemic digestion of Dsg1 by staphylococcal ETs. This observation is specific for patients with SSSS because none of the patients with BI showed any sign of anti-Dsg1 antibody production. This may be because a single episode of BI may be too limited to cause an immune response. Although none of these patients develop PF after SSSS, which is not known as a predisposing factor for PF, the findings presented here provide evidence that infection which modifies self-antigen can trigger the production of IgG autoantibodies against the self-antigen. Of course, these patients do not develop clinically overt PF. We would speculate that other genetic or environmental factors are needed to extend the immune response to encompass pathogenic antibodies and to produce overt clinical PF. For example, in the endemic form of PF, fogo selvagem, that is found in rural areas of South America, it might be possible that repeated modification of Dsg1 by chronic or recurrent staphylococcal infection in genetically susceptible individuals might trigger disease. Thus, our data are consistent with the hypothesis that a bacterial toxin can modify a self-antigen to result in an autoantibody response. The relevance of this finding to onset of autoimmune diseases remains to be proven.