Psoriasis is a skin disease that causes a rash with itchy, scaly patches, most commonly on the knees, elbows, trunk and scalp.
Psoriasis is thought to be an immune system problem that causes skin cells to grow faster than usual. In the most common type of psoriasis, known as plaque psoriasis, this rapid turnover of cells results in dry, scaly patches.
Oliveira ALB, Monteiro VVS; Resveratrol Role in Autoimmune Disease-A Mini-Review. Nutrients. 2017 Dec 1;9(12):1306. doi: 10.3390/nu9121306.
● Models in place 【Date➡Models】
●IL-23 Induced Mice Psoriasis Model
【Mechanism】IL-23 induces CCR6+ γδ T cells, which have the pivotal role in psoriasis-like skin inflammation in mice of producing IL-17A and IL-22.
The intradermal injection of IL-23 represents a mechanistic murine model that recapitulates activation of critical pathways associated with the pathophysiology of psoriasis (ie. production of IL-17 and anti-microbials, alongside epidermal and dermal inflammation) .
●IL-23+IMQ Induced Mice Psoriasis Model
【Mechanism】IL-23 induces CCR6+ γδ T cells, which have the pivotal role in psoriasis-like skin inflammation in mice of producing IL-17A and IL-22.
Imiquimod (IMQ), a Toll-like receptor agonist, forms an immune complex with endogenous molecules when induced, and its interaction with TLR induces the production of type ⅰ IFN-α, leading to psoriasis-like skin injury in its own feedback loop.
●IL-23+IL-36 Induced Mice Psoriasis Model
【Mechanism】IL-23 induces CCR6+ γδ T cells, which have the pivotal role in psoriasis-like skin inflammation in mice of producing IL-17A and IL-22. IL-36 induces the production of CXCL1 and CCL20 from keratinocytes and fibroblasts and attracts neutrophils and T cells; IL-36 upregulates the expression of the keratinocyte mitogens, such as granulocyte colony-stimulating factor and transforming growth factor α in keratinocytes; and IL-36 induces the production of IL-36 in keratinocytes in an autocrine fashion. The released IL-36 upregulates the production of IL-23 from activated DCs, as well as the proliferation and chemokine induction of keratinocytes. The recruited T cells are directed by IL-23 to produce IL-17A and IL-22, and these Th17 cytokines further accelerate keratinocyte proliferation and neutrophilic infiltration.
●IMQ Induced mice Psoriasis Model
【Mechanism】Imiquimod (IMQ), a Toll-like receptor agonist, forms an immune complex with endogenous molecules when induced, and its interaction with TLR induces the production of type ⅰ IFN-α, leading to psoriasis-like skin injury in its own feedback loop.
Topical IMQ treatment is known to exacerbate psoriasis in managed patients, both at the local site of IMQ treatment and distally. In mice, topical IMQ induces a Pso-like disease and is used widely in the field to study basic mechanisms and pharmacological efficacy.
Psoriasis
● Symptoms and Causes
Psoriasis is a skin disease that causes a rash with itchy, scaly patches, most commonly on the knees, elbows, trunk and scalp.
Psoriasis is thought to be an immune system problem that causes skin cells to grow faster than usual. In the most common type of psoriasis, known as plaque psoriasis, this rapid turnover of cells results in dry, scaly patches.
Oliveira ALB, Monteiro VVS; Resveratrol Role in Autoimmune Disease-A Mini-Review. Nutrients. 2017 Dec 1;9(12):1306. doi: 10.3390/nu9121306.
● Models in place 【Date➡Models】
●IL-23 Induced Mice Psoriasis Model
【Mechanism】IL-23 induces CCR6+ γδ T cells, which have the pivotal role in psoriasis-like skin inflammation in mice of producing IL-17A and IL-22.
The intradermal injection of IL-23 represents a mechanistic murine model that recapitulates activation of critical pathways associated with the pathophysiology of psoriasis (ie. production of IL-17 and anti-microbials, alongside epidermal and dermal inflammation) .
●IL-23+IMQ Induced Mice Psoriasis Model
【Mechanism】IL-23 induces CCR6+ γδ T cells, which have the pivotal role in psoriasis-like skin inflammation in mice of producing IL-17A and IL-22.
Imiquimod (IMQ), a Toll-like receptor agonist, forms an immune complex with endogenous molecules when induced, and its interaction with TLR induces the production of type ⅰ IFN-α, leading to psoriasis-like skin injury in its own feedback loop.
●IL-23+IL-36 Induced Mice Psoriasis Model
【Mechanism】IL-23 induces CCR6+ γδ T cells, which have the pivotal role in psoriasis-like skin inflammation in mice of producing IL-17A and IL-22. IL-36 induces the production of CXCL1 and CCL20 from keratinocytes and fibroblasts and attracts neutrophils and T cells; IL-36 upregulates the expression of the keratinocyte mitogens, such as granulocyte colony-stimulating factor and transforming growth factor α in keratinocytes; and IL-36 induces the production of IL-36 in keratinocytes in an autocrine fashion. The released IL-36 upregulates the production of IL-23 from activated DCs, as well as the proliferation and chemokine induction of keratinocytes. The recruited T cells are directed by IL-23 to produce IL-17A and IL-22, and these Th17 cytokines further accelerate keratinocyte proliferation and neutrophilic infiltration.
●IMQ Induced mice Psoriasis Model
【Mechanism】Imiquimod (IMQ), a Toll-like receptor agonist, forms an immune complex with endogenous molecules when induced, and its interaction with TLR induces the production of type ⅰ IFN-α, leading to psoriasis-like skin injury in its own feedback loop.
Topical IMQ treatment is known to exacerbate psoriasis in managed patients, both at the local site of IMQ treatment and distally. In mice, topical IMQ induces a Pso-like disease and is used widely in the field to study basic mechanisms and pharmacological efficacy.
