The extent of desmoglein 3 depletion in pemphigus vulgaris is dependent on Ca(2+)-induced differentiation: a role in suprabasal epidermal skin splitting?

@article{Spindler2011TheEO,
  title={The extent of desmoglein 3 depletion in pemphigus vulgaris is dependent on Ca(2+)-induced differentiation: a role in suprabasal epidermal skin splitting?},
  author={Volker Spindler and Alexander Endlich and Eva Hartlieb and Franziska Vielmuth and Enno Schmidt and Jens Waschke},
  journal={The American journal of pathology},
  year={2011},
  volume={179 4},
  pages={1905-16}
}
Pemphigus vulgaris (PV) is an autoimmune disease of the skin and mucous membranes and is characterized by development of autoantibodies against the desmosomal cadherins desmoglein (Dsg) 3 and Dsg1 and formation of intraepidermal suprabasal blisters. Depletion of Dsg3 is a critical mechanism in PV pathogenesis. Because we did not detect reduced Dsg3 levels in keratinocytes cultured for longer periods under high-Ca(2+) conditions, we hypothesized that Dsg depletion depends on Ca(2+)-mediated… CONTINUE READING

Citations

Publications citing this paper.
Showing 1-10 of 11 extracted citations

Pemphigus, a pathomechanism of acantholysis.

The Australasian journal of dermatology • 2017
View 1 Excerpt

References

Publications referenced by this paper.
Showing 1-10 of 55 references

p38MAPK inhibition prevents disease in pemphigus vulgaris mice.

Proceedings of the National Academy of Sciences of the United States of America • 2006
View 9 Excerpts
Highly Influenced

Similar Papers

Loading similar papers…