Sammendrag
Psoriasis is a human chronic, immune disease with severe cutaneous and systemic manifestations. Its prevalence, among the world population, highly varies with ethnicity and geography, but not sex from remarkable low levels in Asia to 2.3% in Spain, or an impressive 11.5% in Norway. The pathogenesis of psoriasis derives from complex genetic and environmental interactions, which creates aberrant crosstalk between keratinocytes and variated immune cell, resulting in open amplified inflammatory and pro-proliferative circuits. Both, innate and adaptive immune systems are known to be involved in the response at the cellular and humoral levels. Nevertheless, the exact molecular mechanisms are still under debate. Therefore, discovering useful therapeutic targets to stretch the molecular gaps in psoriasis pathogenesis and its associated comorbidities is still mandatory. So far, some mutagenic or pharmacological studies in vitro or using comparative vertebrate models have provided critical molecular insights and directed the human research. Although highly feasible in rodents, the versatile physiology, genetic similarity to humans and outstanding molecular toolbox available, suggest that elaborate forward genetic screenings are far easier to be conducted using the zebrafish model. Thus, in this review, we intend to briefly overview psoriasis and revise in a digested fashion the preclinical research models available, emphasizing the zebrafish as a powerful tool in the study of immune effectors on the same, and how it supports the discovering of new therapies that may help in controlling this widespread disease around the globe.
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