@article{98197,
  keywords = {IL-10, PD-1, T cell anergy, T cells, Tregs, leprosy},
  author = {Tarique M and Naz H and Suhail M and Turan A and Saini C and Muhammad N and Shankar H and Zughaibi T and Khan T and Khanna N and Sharma A},
  title = {Differential expression of programmed death 1 (PD-1) on various immune cells and its role in human leprosy.},
  abstract = {<p>Leprosy is a chronic bacterial disease caused by&nbsp;<em>Mycobacterium leprae</em>. Leprosy patients have been found to have defects in T cells activation, which is critical to the clearance of the bacilli. Treg cell suppression is mediated by inhibitory cytokines such as IL10, IL-35 and TGF-β and its frequency is higher in leprosy patients. Activation and overexpression of programmed death 1 (PD-1) receptor is considered to one of the pathways to inhibit T-cell response in human leprosy. In the current study we address the effect of PD-1 on Tregs function and its immuno-suppressive function in leprosy patients. Flow cytometry was used to evaluate the expression of PD-1 and its ligands on various immune cells T cells, B cells, Tregs and monocytes. We observed higher expression of PD-1 on Tregs is associated with lower production of IL-10 in leprosy patients. PD-1 ligands on T cells, B cells, Tregs and monocytes found to be higher in the leprosy patients as compared to healthy controls. Furthermore, blocking of PD-1 restores the Tregs mediated suppression of Teff and increase secretion of immunosuppressive cytokine IL-10. Moreover, overexpression of PD-1 positively correlates with disease severity as well as Bacteriological Index (BI) among leprosy patients. Collectively, our data suggested that PD-1 overexpression on various immune cells is associated with disease severity in human leprosy. Manipulation and inhibition of PD-1 signaling pathway on Tregs alter and restore the Treg cell suppression activity in leprosy patients.</p>
},
  year = {2023},
  journal = {Frontiers in immunology},
  volume = {14},
  pages = {1-10},
  month = {04/2023},
  issn = {1664-3224},
  url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10161389/pdf/fimmu-14-1138145.pdf},
  doi = {10.3389/fimmu.2023.1138145},
  language = {eng},
}