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Failure in regulatory mechanisms triggers a complex network of dynamic relationships between innate and adaptive immunity, leading to coexistent autoinflammatory and autoimmune processes. Sustained exposure to a trigger or a genetic alteration at the level of the receptors of the natural immune system may lead to abnormal activation of the innate immune system, adaptive system activation, loss of self\u2010tolerance, and systemic inflammation. The IL\u20101 family members critically activate and regulate innate and adaptive immune responses\u2019 diversity and plasticity in autoimmune and\/or autoinflammatory conditions. The IL\u201023\/IL\u201017 axis is key in the communication between innate immunity (IL\u201023\u2010producing myeloid cells) and adaptive immunity (Th17\u2010 and IL\u201017\u2010expressing CD8+ T cells). In psoriasis, these cytokines are decisive to the different clinical presentations, whether as plaque psoriasis (psoriasis vulgaris), generalized pustular psoriasis (pustular psoriasis), or mixed forms. 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