"Haptens, antigens and superantigens can all induce AD animal models.
[Modeling mechanism] Small molecule haptens combine with proteins in the body to form a complete antigen, which is absorbed by Langerhans cells. The corresponding antigen is presented to T cells and activated, and contact dermatitis occurs again
Although the superantigen produced by the major histocompatibility gene complex type II (MHCII) molecule exists, it does not act on the antigen binding groove of the MHC, and a complete superantigen can bind to it. Conserved amino acid residues outside the antigen binding groove; special antigen-presenting cells induced by cytokines; or direct binding with non-specialized antigen-presenting cells can activate inflammatory response; superantigens can activate B lymphocytes or stimulate T cell activation, thereby The lymphocytes that expand specific T cells can also express the receptor VB area and affect inflammation and autoimmunity
[Model Features] The commonly used hapten is dinitrochlorobenzene Nc/Nga mouse foot pads. The abdomen is repeatedly applied dinitrochlorobenzene to the ears and back for 7 weeks. The skin of the test site shows an AD-like appearance, such as Erythema, exudation, shedding, etc.; in the histopathological section, it is found that the epidermis is thickened, there are corneal proliferative diseases, intercellular edema and a large number of inflammatory cells. Infiltration of the epidermis and dermis; increased levels of IL-4 and IgE in the blood; this is an allergen that can exacerbate the disease; after multiple transdermal administrations, local hypertrophy of the spinal cord, epidermal spongiform edema, and skin vasodilation With the proliferation and congestion of collagen fibers, the increase of eosinophils, the infiltration of neutrophils, plasma cells and lymphocytes, the level of total serum IgE increased significantly, and the expression of IL-4 and IL-5 mRNA in the skin lesions Significantly increased. Significant changes in IFN mRNA indicate the existence of Th2-mediated cellular immunity in skin damage. Applying the superantigen Langerhans cell enterotoxin B to the back of BALB/c mice can cause changes in dermatitis, acid bulb infiltration and obese cells Proliferation occurs at the test site, their number is positively correlated with superantigen colonization or infection, and IL-13 mRNA expression is significantly increased. Partial use is also included. Of particular interest is that mixing milk or peanuts with cholera helper toxins can also cause AD in female C3H/HeJ mice. Phenotype. This model is the first animal AD model obtained by tube feeding, which provides a suitable mouse model for further research on food-induced AD. [Model Evaluation and Application] The biggest advantage of antigen-induced AD animal models is that they can be repeatedly established. Secondly, this type of model reflects the diversity and complexity of the causes of AD from different perspectives, and can be fully understood. It provides an excellent platform to find the cause and treatment of AD mechanism.