Psoriasis is an immune mediated inflammatory skin disease caused by a complex interplay between the immune system, Psoriasis-associated susceptibility loci, Psoriasis autoantigens and multiple environmental factors. Over the last two decades, researches has unequivocally shown that 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 produces a feed forward inflammatory response in keratinocytes that is self-amplifying and drives the development of mature psoriatic plaques by inducing epidermal hyperplasia, epidermal cell proliferation and the recruitment of leukocyte subsets into the skin. The discovery of the central role for the IL- 23/Th17 cell axis in the development of Psoriasis has led to a major paradigm shift in the pathogenic model for this condition [1,2].

References

1. Fitch E., et al. “Pathophysiology of psoriasis: recent advances on IL-23 and Th17 cytokines”. Current Rheumatology Reports6 (2007): 461-467.
2. Davidovici BB., et al. “Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions”. Journal of Investigative Dermatology 7 (2010):1785-1796.
3. Hawkes JE., et al. “Psoriasis pathogenesis and the development of novel targeted immune therapies”. Journal of Allergy and Clinical Immunology3 (2017): 645-653.
4. Nestle FO., et al. “Plasmacytoid predendritic cells initiate psoriasis through interferon-α production”. Journal of Experimental Medicine1 (2005): 135-143.
5. Elder JT. “Genome-wide association scan yields new insights into the immunopathogenesis of psoriasis”. Genes and Immunity3 (2009): 201.

Citation

Citation: Shirin Tarafder . “IL-23/Th17 Cell Axis and Psoriasis".Acta Scientific Microbiology 3.1 (2020): 48-49.

Copyright

Copyright: © 2020 Lia Shirin Tarafder. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.