Final answer:
During the subacute/chronic phase of Canine Atopic Dermatitis (cAD), there is a TH1 cytokine-mediated inflammatory response that leads to skin lesions or contact dermatitis. Memory T cells release cytokines upon exposure to antigens, activating macrophages which cause tissue damage. Treatment often involves cortisone to inhibit cytokine production and alleviate symptoms.
Step-by-step explanation:
Canine Atopic Dermatitis (CAD) is a type of hypersensitivity reaction seen in dogs, which can manifest in various stages, including acute, subacute, and chronic. During the subacute/chronic phase of cAD, there is a cell-mediated immune response that can take one to two days after secondary exposure for a maximal reaction to occur. This type of hypersensitivity involves a TH1 cytokine-mediated inflammatory response, which may result in local tissue lesions or contact dermatitis, presenting as a rash or skin irritation.
Detailed hypersensitivity mechanisms include the sensitization phase, where antigens are introduced to the skin and processed by antigen-presenting cells (APCs). These APCs then activate helper T cells, promoting clonal proliferation and differentiation into memory T1 cells. Upon subsequent antigen exposure, these sensitized memory T1 cells release cytokines that activate macrophages. Activated macrophages are responsible for tissue damage seen in hypersensitivity, such as in contact dermatitis and tuberculin reaction.
In cases like contact sensitivity reactions due to substances such as nickel or poison ivy, the symptoms may be more severe due to the added toxicity of the oils of the plant in the case of poison ivy, but treatments often revolve around the use of cortisone to inhibit cytokine production and resolve symptoms.