Nancy Sinha

Centre for Psoriasis

Psoriasis is a chronic autoimmune disease that causes red, itchy, and scaly patches on the skin. Such patches can be formed anywhere on the body but typically occur on the inside of the elbows, knees, and scalp.

Psoriasis is caused by a complex interplay between the immune system, psoriatic-associated susceptibility loci, autoantigens, and multiple environmental factors. Psoriasis represents a T cell-mediated disease primarily driven by pathogenic T cells that produce high levels of IL-17 in response to IL-23.

The activation and upregulation of IL-17 in pre-psoriatic skin produce a “feed-forward” inflammatory response in keratinocytes. It is self-amplifying and drives the development of mature psoriatic plaques by inducing epidermal hyperplasia, epidermal cell proliferation, and recruitment of leukocyte subsets into the skin.

Psoriasis can be triggered by various factors in genetically susceptible individuals, including trauma, infection (such as streptococcal infection), and medications.

Many abnormalities have been observed involving antigen presentation, activation of NF-Kb signaling pathways, differentiation of T helper cell populations, and enhanced IL-17 response and infiltration of immune cells.

IL-22 and IL-23 stimulate bone formation while Tumor Necrosis Factor (TNF) enhances bone resorption and the IL-17A stimulates both processes.