Atopic dermatitis patients clinically present skin erythematous plaques, eruption, elevated serum IgE and T helper cell type 2(Th2) cytokine levels, such as IL-4 and IL-13. Microscopically, atopic dermatitis patients also show epidermal hyperplasia and accumulation of mast cells and Th2.
In some people, atopic dermatitis is related to a gene variation that affects the skin's ability to provide protection. In other people, atopic dermatitis is caused by too much of the bacteria Staphylococcus aureus on the skin.
Guttman-Yassky E, Dhingra N, Leung DY. New era of biologic therapeutics in atopic dermatitis. Expert Opin Biol Ther. 2013;13(4):549-561.
● Models in place 【Date➡Models】
●DNCB Induced AD Model
【Mechanism】Haptens are small molecule irritants that bind to proteins and elicit an immune response and have long been used to study allergic contact dermatitis (ACD). Repeated hapten challenges disrupt the skin barrier, combined with a Th2-biased immune response.
The majority of haptens, such as 2,4-dinitrochlorobenzenen(DNCB) and oxazolone(OXA), induce a response shift from Th1 to Th2 is observed following repeated application of hapten, in other words, contact dermatitis to atopic dermatitis-like skin lesion.
●OXA Induced AD Model
【Mechanism】Haptens are small molecule irritants that bind to proteins and elicit an immune response and have long been used to study allergic contact dermatitis (ACD). Repeated hapten challenges disrupt the skin barrier, combined with a Th2-biased immune response.
The majority of haptens, such as 2,4-dinitrochlorobenzenen(DNCB) and oxazolone(OXA), induce a response shift from Th1 to Th2 is observed following repeated application of hapten, in other words, contact dermatitis to atopic dermatitis-like skin lesion.
●MC903 Induced AD Model
【Mechanism】MC903 (calcipotriol) is an active vitamin D analog without affecting calcium metabolism and has been used for psoriasis patients. It induces irritant skin inflammation in some psoriasis patients as a side effect.
In mice MC903 upregulates TSLP and induces atopic disease-like skin inflammation in a TSLP-dependent manner. Collectively, the MC903 model allows us to explore how type 2 skin inflammations are initiated by TSLP and to analyze the roles of various immune cells especially in the early period of inflammations.
●FITC Induced BALB/c AD Model
【Mechanism】The mice showed normal migration and maturation of skin dendritic cells and induction of hapten-specific T cells in the sensitization phase of FITC-induced AD, and normal induction of local inflammation in the elicitation phase of FITC-induced AD. On the other hand, those mice showed reduced scratching frequency and duration during FITC-induced AD.
Atopic Dermatitis (AD)
● Symptoms and Causes
Atopic dermatitis patients clinically present skin erythematous plaques, eruption, elevated serum IgE and T helper cell type 2(Th2) cytokine levels, such as IL-4 and IL-13. Microscopically, atopic dermatitis patients also show epidermal hyperplasia and accumulation of mast cells and Th2.
In some people, atopic dermatitis is related to a gene variation that affects the skin's ability to provide protection. In other people, atopic dermatitis is caused by too much of the bacteria Staphylococcus aureus on the skin.
Guttman-Yassky E, Dhingra N, Leung DY. New era of biologic therapeutics in atopic dermatitis. Expert Opin Biol Ther. 2013;13(4):549-561.
● Models in place 【Date➡Models】
●DNCB Induced AD Model
【Mechanism】Haptens are small molecule irritants that bind to proteins and elicit an immune response and have long been used to study allergic contact dermatitis (ACD). Repeated hapten challenges disrupt the skin barrier, combined with a Th2-biased immune response.
The majority of haptens, such as 2,4-dinitrochlorobenzenen(DNCB) and oxazolone(OXA), induce a response shift from Th1 to Th2 is observed following repeated application of hapten, in other words, contact dermatitis to atopic dermatitis-like skin lesion.
●OXA Induced AD Model
【Mechanism】Haptens are small molecule irritants that bind to proteins and elicit an immune response and have long been used to study allergic contact dermatitis (ACD). Repeated hapten challenges disrupt the skin barrier, combined with a Th2-biased immune response.
The majority of haptens, such as 2,4-dinitrochlorobenzenen(DNCB) and oxazolone(OXA), induce a response shift from Th1 to Th2 is observed following repeated application of hapten, in other words, contact dermatitis to atopic dermatitis-like skin lesion.
●MC903 Induced AD Model
【Mechanism】MC903 (calcipotriol) is an active vitamin D analog without affecting calcium metabolism and has been used for psoriasis patients. It induces irritant skin inflammation in some psoriasis patients as a side effect.
In mice MC903 upregulates TSLP and induces atopic disease-like skin inflammation in a TSLP-dependent manner. Collectively, the MC903 model allows us to explore how type 2 skin inflammations are initiated by TSLP and to analyze the roles of various immune cells especially in the early period of inflammations.
●FITC Induced BALB/c AD Model
【Mechanism】The mice showed normal migration and maturation of skin dendritic cells and induction of hapten-specific T cells in the sensitization phase of FITC-induced AD, and normal induction of local inflammation in the elicitation phase of FITC-induced AD. On the other hand, those mice showed reduced scratching frequency and duration during FITC-induced AD.
