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Psoriasis is a chronic autoimmune disease primarily affecting the skin and often joints. The worldwide prevalence is estimated at 2-3%, approximately 125 million people (2015). The overall incidence of psoriasis is also high and increasing over time. In a retrospective cohort of adults, the incidence increased from 50.8 cases per 100,000 population between 1970–1974 to 100.5 cases per 100,000 individuals between 1995–1999. Psoriasis commonly develops between the ages of 15 and 35, but it can develop at any age, even in infants. About 10-15% of those with psoriasis get it before 10 years of age. Women and men are affected equally.

It has several phenotypes, most common being psoriasis vulgaris. Psoriasis like other autoimmune diseases- for example Type 1 Diabetes Mellitus- has strong genetic components located in the HLA regions. One such loci is psoriasis susceptibility locus 1 (PSORS1). The strongest HLA-related associations in psoriasis have consistently mapped to HLA-C*06 in the white population. The disease is characterised by remission and flare-up again similar to the ‘attack and retreat’ of the autoimmune destruction in Type 1 Diabetes Mellitus or Multiple Sclerosis. The prevalence of psoriasis among first-degree relatives is high ~4-19%, higher than in the general population- another similarity with Type 1 Diabetes Mellitus.

Its pathophysiology is characterised by abnormal keratocyte proliferation and immune cell infiltration in the epidermis and dermis. The abnormal recognition and presentation of putative autoantigen/s triggers autoaggressive T cell populations, Th1 and Th17 being key players. The disease is maintained and exacerbated by pro-inflammatory cytokines (TNF-alpha, IL-17, IL-22 and 23, CCL20). Epithelial damage triggers anti-microbial peptides such as CAMP which then mediates plasmacytoid dentritic cell (pDC) activation further fuelling the skin destruction. Nevertheless, the identities of the autoaggressive immune cells as well as the putative targeted self-antigen/s remain to be discovered.

There is no cure for psoriasis. Diagnosis is straightforward in most cases. It is based on medical history, physical exam and skin biopsy performed occasionally for confirmation. In psoriasis vulgaris the skin develops patches, which are dry, itchy, red and covered with silver scales. Current treatments are aimed at reducing inflammation in order to clear the skin. Topical medication (creams, ointments), light therapy (UV light, A or B)) and systemic drugs are used to provide some relief. Systemic drugs are immunosuppressive agents (Methotrexate, Cyclosporine etc..) with significant potential side-effects. More recently drugs called biologics have been used. These are tumor necrosis factor (TNF)-α inhibitors (e.g. etanercept, adalimumab) and interleukin-12/23 inhibitors (e.g. ustekinumab).

PHAIM Ltd has been created on a unique immune modulatory platform to treat and cure autoimmune diseases. The key is to reintroduce the self-antigen in a special formulation which downregulates autoaggressive T cells and stimulates the regulatory immune cells to regain control and re-establish the healthy immune balance. Our Antigenic Immune Modulator (AIM) therapy is based on disease specific antigens. It is a potential game changer, a curative approach in psoriasis.

Therapeutic Market - Psoriasis