This skin disease with a pattern of inflammatory skin in which the epidermis is thickened. The lesions are epidermal thickenings which reflect excessive epidermal cell proliferation (McPhee & Hammer, 2010). The reason for excessive cell production is from the shortened lifespan of the keratinocyte cell cycle. Psoriasis also causes endothelial cell hyperproliferation that causes pronounced vasculature in the superficial dermis (McPhee & Hammer, 2010). Research has shown that psoriasis creates an antigen that is established as a ligand for T-cells and CD8 lymphocytes. Also there is shown to be an overexpression of Interleukin-2 (IL-2) may cause metastatic malignancies (McPhee & Hammer, 2010). Cytotoxic T lymphocytes (CTL) eliminate target cells and differ from helper T lymphocytes by having the CD8 surface antigen. This allows CTLs to bind and induce apoptosis. There are come CTLs that live longer to provide a “recall” response to latent or chronic inflammatory processes which lacks in psoriasis. IgG and IgM are antibodies that bind to cell structures which signals for cell destruction. Psoriasis has an over proliferation of these antibodies which creates scars on the skin over a length of time.
Post a 2 paragraph in response to above post about either….
· Share insights on how Age, genetics, or gender impacts the pathophysiology of the above immune disorder
· Expanding on the posting by providing additional insights or contrasting perspectives based on readings and evidence.