Author(s): Deepak H B, Sabina Evan Prince


DOI: 10.5958/0974-360X.2017.00491.7   

Address: Deepak H B, Sabina Evan Prince*
School of Biosciences and Technology, VIT University, Vellore-632014, Tamilnadu, India
*Corresponding Author

Published In:   Volume - 10,      Issue - 8,     Year - 2017

Autoimmunity is the process of immune responses of an organism against its own tissues and cells. Autoimmune disorders have been strongly associated with genetic, infectious, and environmental predisposing factors. Psoriasis is a chronic inflammatory skin disease, characterized by T cell-mediated hyper-proliferation of keratinocytes, affecting about 2% of the worldwide population. Psoriasis is associated with a high degree of morbidity; patients are embarrassed about the appearance of their skin, and there are side effects of medications. Its prevalence is equal in men and women and can first appear at any age, from infancy to elderly, although the mean age of development has suggested being around 30 years old. To control the development of autoimmunity, multiple mechanisms of peripheral tolerance have evolved. PD-1 is a member of the CD28/CTLA-4/ICOS co-stimulatory receptor family, delivers negative signals that have profound effects on T cell immunity. The PD-1/PD-L1 interaction inhibits T-lymphocyte proliferation, release of cytokines, and cytotoxicity, resulting in exhaustion and apoptosis of tumour specific T cells. Many new findings on T cells and their contributions to the disease development have challenged our conventional views regarding psoriasis as a T helper (Th) 1-mediated skin disease and prompted us to reassess T-cell functions in psoriasis. The PD-1: PDL signalling pathway has been shown to play an important role in a variety of diseases, including autoimmune conditions like type 1 diabetes, MS, AD, psoriasis, and cancer.

Cite this article:
Deepak H B, Sabina Evan Prince. A Systematic Review on the Role of PD-1 and its Ligands in Autoimmunity. Research J. Pharm. and Tech. 2017; 10(8): 2771-2776. doi: 10.5958/0974-360X.2017.00491.7

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DOI: 10.5958/0974-360X 

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