While conventionally the skin is recognised as a passive anatomical shield, recent research suggests that the role of skin goes far beyond protection and perception. Skin may be actively coordinating with body’s immune responses.
The research included collaborators from the Chinese Academy of Medical Sciences Institute of Dermatology and Tsinghua’s School of Pharmaceutical Sciences found that keratinocytes ( cells found in the outer layer of skin) upon detection of local stress such as infection or UV damage produce a metabolic molecule called farnesyl pyrophosphate (FPP) .
FPP binds to and activates a protein channel called TRPV3(Transient Receptor Potential Vanilloid 3, a heat and chemical sensitive ion channel found in skin cells that helps trigger signalling processes, including immune responses and causes calcium influx). This signalling cascade stimulates the production of the immune mediators IL-6 and CCL20.
IL-6 supports the development of T follicular helper cells, while CCL20 attracts migratory dendritic cells to the draining lymph nodes. Together, these signals boost germinal centre reactions, leading to production of pathogen specific IgG antibodies and the formation of long lived memory B cells and plasma cells.
A companion study identified that natural aromatic compounds Carvacrol and Camphor, can activate the TRPV3 pathway. When given locally with an antigen, the compounds significantly increased antigen specific IgG responses in a dose dependent manner, with no observed toxicity at effective doses in mouse models.
Therapeutic and vaccine implications.
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TRPV3 and its effectors( IL-6 and CCL20) can be used a therapeutic targets for autoimmune diseases like systemic lupus erythematous.
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The natural compounds may offer a targeted and safer alternative for mucosal vaccine delivery
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This study can provide foundation for developing next generation immunotherapies.
In the future, the key to controlling immunity may not lie deep within the body, but on the surface of our skin.
MBH/AB