The skin is a major component of the integumentary system and forms a defensive barrier that protects the internal environment against external forces (Seeley, 2008). Studies carried out by Lowes, Suárez-Fariñas, and Krueger (2013), Cargill et al. (2007) and Tsoi et al. (2012) show that psoriasis vulgaris is a homeostatic disorder of the skin that interrupts the normal proliferation, differentiation and maturation of epithelial cells in the stratum corneum. The focul site of psoriasis vulgaris, called psoriatic, lesions contain higher than normal levels of T Cells, leading to the conclusion that psoriasis vulgaris is a T Cell mediated response to external triggers of either the skin or the immune system (Roberson & Bowcock, 2010; Sabat &
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The lesions may diminish in-time however psoriasis vulgaris is classified by a re-emergence and ongoing flare-ups (Griffiths & Barker, 2007). There are several recognised forms of psoriasis such as sebhorric psoriasis, nail psoriasis, inverse psoriasis, guttate psoriasis and pustular psoriasis; however psoriasis vulgaris is the most common form of the skin disorder with 90% of cases reportedly of psoriasis vulgaris (Parisi, Symmons, Griffiths, & Ashcroft, …show more content…
The abnormal T Cell mediated response results in a hyper-proliferation of epithelial cells and as a result the keratinocyte is not able to follow the normal process of differentiation and maturation (Nograles, Davidovici, & Krueger, 2010; Sabat & Wolk, 2011). The cells reaching the superficial layers of the stratum corneum in psoriatic skin have not yet fully matured into corneocytes. The layers of immature cells accumulate on the surface of the skin to form psoriatic lesions which contain higher than normal levels of T Cells (Ghadially et al., 1996; Lowes et al., 2008; Lowes et al., 2013; Nograles et al., 2010).
Psoriasis vulgaris is said by Lowes et al. (2013) to be “…a disease mediated by activated T Cells that are present in focal skin regions…” (Lowes, M., Suárez-Fariñas, M., Krueger, J., 2013, Immunology of Psoriasis Annual Review of Immunology; 32: 227–255). But it is unclear whether the genetic foundation for the abnormality is of the skin itself or the immune system (Roberson & Bowcock, 2010). It is generally agreed up that the normal homeostatic repair of the skin’s barrier, in psoriatic skin, is malfunctioning and there is a defective immune response to irritation (Lowes et al., 2008; Sabat & Wolk,
The lesions may diminish in-time however psoriasis vulgaris is classified by a re-emergence and ongoing flare-ups (Griffiths & Barker, 2007). There are several recognised forms of psoriasis such as sebhorric psoriasis, nail psoriasis, inverse psoriasis, guttate psoriasis and pustular psoriasis; however psoriasis vulgaris is the most common form of the skin disorder with 90% of cases reportedly of psoriasis vulgaris (Parisi, Symmons, Griffiths, & Ashcroft, …show more content…
The abnormal T Cell mediated response results in a hyper-proliferation of epithelial cells and as a result the keratinocyte is not able to follow the normal process of differentiation and maturation (Nograles, Davidovici, & Krueger, 2010; Sabat & Wolk, 2011). The cells reaching the superficial layers of the stratum corneum in psoriatic skin have not yet fully matured into corneocytes. The layers of immature cells accumulate on the surface of the skin to form psoriatic lesions which contain higher than normal levels of T Cells (Ghadially et al., 1996; Lowes et al., 2008; Lowes et al., 2013; Nograles et al., 2010).
Psoriasis vulgaris is said by Lowes et al. (2013) to be “…a disease mediated by activated T Cells that are present in focal skin regions…” (Lowes, M., Suárez-Fariñas, M., Krueger, J., 2013, Immunology of Psoriasis Annual Review of Immunology; 32: 227–255). But it is unclear whether the genetic foundation for the abnormality is of the skin itself or the immune system (Roberson & Bowcock, 2010). It is generally agreed up that the normal homeostatic repair of the skin’s barrier, in psoriatic skin, is malfunctioning and there is a defective immune response to irritation (Lowes et al., 2008; Sabat & Wolk,