Psoriasis is an inflammatory skin disease mediated by both innate and adaptive immune systems. The skin contains skin-associated lymphoid tissue (SALT), which includes immune cells like T cells and dendritic cells. In psoriasis, inflammatory myeloid dendritic cells release IL-23 and IL-12, activating IL-17-producing T cells, Th1 cells, and Th22 cells, leading to the production of psoriatic cytokines such as IL-17, IFN-γ, TNF, and IL-22. These cytokines mediate effects on keratinocytes, amplifying psoriatic inflammation. Anticytokine antibodies have shown the importance of IL-23, TNF, and IL-17 in this process. The genetic background of psoriasis is linked to immune function, including key PSORS loci, single nucleotide polymorphisms, and the skin transcriptome. Comorbidities such as psoriatic arthritis, depression, and cancer are associated with psoriasis. Psoriasis-related cytokine-response pathways are considered in the context of the transcriptome of different mouse models. This approach offers a model for other inflammatory skin and autoimmune diseases. Psoriasis is characterized by thickened epidermis, hyperkeratosis, and inflammatory infiltrates. The initiation phase of psoriasis involves injury, infection, or medications, leading to the activation of immune cells. Studies have shown that psoriasis is a T cell-mediated disease, with activated T cells producing cytokines that drive inflammation. Myeloid dendritic cells play a key role in psoriasis by activating T cells and producing cytokines. T cells in psoriasis lesions produce IL-17, IFN-γ, and TNF, contributing to inflammation. Keratinocytes respond to these cytokines by upregulating inflammatory products, leading to a self-amplifying loop of inflammation. Genetic mutations, such as in CARD14 and IL36RN, are associated with psoriasis. These mutations affect immune pathways and contribute to the disease. The integration of genetics and the transcriptome of psoriasis reveals immune pathways involved in the disease. Comorbidities in psoriasis include cardiovascular risk, diabetes, and metabolic syndrome, which are correlated with psoriasis severity. The causal relationship between psoriasis and systemic comorbidities is not fully understood, but shared genetic risks and inflammatory pathways may provide links. The skin transcriptome and serum protein measurements in psoriasis patients show elevated levels of inflammatory cytokines and chemokines, supporting a model of systemic inflammation.Psoriasis is an inflammatory skin disease mediated by both innate and adaptive immune systems. The skin contains skin-associated lymphoid tissue (SALT), which includes immune cells like T cells and dendritic cells. In psoriasis, inflammatory myeloid dendritic cells release IL-23 and IL-12, activating IL-17-producing T cells, Th1 cells, and Th22 cells, leading to the production of psoriatic cytokines such as IL-17, IFN-γ, TNF, and IL-22. These cytokines mediate effects on keratinocytes, amplifying psoriatic inflammation. Anticytokine antibodies have shown the importance of IL-23, TNF, and IL-17 in this process. The genetic background of psoriasis is linked to immune function, including key PSORS loci, single nucleotide polymorphisms, and the skin transcriptome. Comorbidities such as psoriatic arthritis, depression, and cancer are associated with psoriasis. Psoriasis-related cytokine-response pathways are considered in the context of the transcriptome of different mouse models. This approach offers a model for other inflammatory skin and autoimmune diseases. Psoriasis is characterized by thickened epidermis, hyperkeratosis, and inflammatory infiltrates. The initiation phase of psoriasis involves injury, infection, or medications, leading to the activation of immune cells. Studies have shown that psoriasis is a T cell-mediated disease, with activated T cells producing cytokines that drive inflammation. Myeloid dendritic cells play a key role in psoriasis by activating T cells and producing cytokines. T cells in psoriasis lesions produce IL-17, IFN-γ, and TNF, contributing to inflammation. Keratinocytes respond to these cytokines by upregulating inflammatory products, leading to a self-amplifying loop of inflammation. Genetic mutations, such as in CARD14 and IL36RN, are associated with psoriasis. These mutations affect immune pathways and contribute to the disease. The integration of genetics and the transcriptome of psoriasis reveals immune pathways involved in the disease. Comorbidities in psoriasis include cardiovascular risk, diabetes, and metabolic syndrome, which are correlated with psoriasis severity. The causal relationship between psoriasis and systemic comorbidities is not fully understood, but shared genetic risks and inflammatory pathways may provide links. The skin transcriptome and serum protein measurements in psoriasis patients show elevated levels of inflammatory cytokines and chemokines, supporting a model of systemic inflammation.