Psoriasis is a heterogeneous disorder with many different phenotypes. Further, different forms may alter their morphology and course of disease in that, for instance, plaque-type psoriasis may become pustular and vice versa. With advancing insight in immunopathology phenotype switching can now be explained by directional changes from T cell-mediated pathology to an inflammatory neutrophilic pattern which is driven by innate signalling. Within this framework not a single 'antigen' but various causative agents play a key role.
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Enno Christophers (2007) studied this question.
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