Centre for Skin Diseases

VV Biotech has discovered a drug that contains RNA and by using this drug the pathway associated with autoimmune skin diseases can be down regulated.

We hypothesize that quantification of target gene miRNA expression in genes may be useful. It also can be a non-invasive approach to monitor the disease activity as well as treatment response of all autoimmune skin diseases.

There are about 1500 distinct skin diseases and few more variants that could be found in an average 15% population related to skin problems. Moreover, it is said that 50 to 75% of individuals may have skin problems at any time in their lives.

We are trying to down regulate pathways associated with interleukins, interferon, and cytokines based on our studies. The targets we have studied includes- IL17, 17A, IL-1,2,4,5,6,12,22,23,33, TLR-6,7,8,9, CD20,40, 151, IFNα, IFNϒ, TNFα, NFkβ, MMP-9,13, CDK-N1α, CDK-1β, and CDKN2A.

These specific pathways could serve as drug targets for chronic and acute skin fibrosis conditions.

Significant diseases- Psoriasis, Lupus of the skin, Morphea/Scleroderma, Eczemas burn, Bechet’s disease, Lichen planus, Dermatomyositis, Pemphigoid.

Systematic therapies- Immunomodulators, and a few novel injectable products.

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.