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\begin{document}

\title{PD-1/PD-L1 and PD-1/PD-L2 axes-targeted anti-leishmanial therapy}



\author[1]{Abdollah Jafarzadeh}%
\author[2]{Sunil Kumar}%
\author[2]{Neelam Bodhale}%
\author[3]{Sarah Jafarzadeh}%
\author[1]{Maryam Nemati}%
\author[1]{Iraj Sharifi}%
\author[4]{Arup Sarkar}%
\author[2]{BHASKAR SAHA}%
\affil[1]{Kerman University of Medical Sciences}%
\affil[2]{National Centre for Cell Science}%
\affil[3]{Kerman University of Medical Sciences, Kerman, Iran. }%
\affil[4]{Trident Academy of Creative Technology}%


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  \date{May 24, 2024}


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\begin{abstract}
Although programmed cell death protein-1 (PD-1) is expressed on CD4+ T,
CD8+ T and B cells, the T cell expression of PD-1 and macrophages'
expression of its ligands- PD-L1 and PD-L2 increase during
leishmaniasis. The PD-1/PD-L1 interaction induces T cell anergy, T cell
apoptosis and exhaustion, diversion of T cells toward TH2 and T-reg
cells and inhibition of M1 macrophage activities by suppression of
nitric oxide (NO) and reactive oxygen species (ROS) production. These
changes exacerbate Leishmania infection. As PD-L1-deficient, but not
PD-L2-deficient, mice were protected against L. mexicana infection,
differential roles have been proposed for PD-L1 and PD-L2 in mouse
models of leishmaniasis. Blockade of PD-1/PD-L1 interaction in various
in vitro and Leishmania-infected mouse, hamster and dog models enhanced
IFN-\selectlanguage{greek}γ \selectlanguage{english}and NO production, reduced IL-10 and TGF-\selectlanguage{greek}β \selectlanguage{english}generation, promoted T
cell proliferation and decreased parasite burden. Blockage of PD-1/PD-L1
axis can be considered as a potential therapeutic strategy to restore
protective immunity during leishmaniasis, particularly in drug-resistant
cases.%
\end{abstract}%



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