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\begin{document}

\title{Modulation of hematopoiesis by protozoal and helminth parasites}



\author[1]{Kyle Cunningham}%
\author[2]{Kingston Mills}%
\affil[1]{University of Glasgow}%
\affil[2]{Academic Director Trinity Biomedical Sciences Institute  TCD Research Theme Leader Immunology, Inflammation and Infection  School of Biochemistry and Immunology  Trinity Biomedical Sciences Institute  Trinity College Dublin, Ireland}%


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  \date{June 08, 2024}


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\begin{abstract}
During inflammation hematopoietic stem cells (HSCs) in the bone marrow
(BM) and periphery rapidly expand and preferentially differentiate into
myeloid cells that mediate innate immune responses. HSCs can be directed
into quiescence or differentiation by sensing alterations to the
hematopoietic niche, including cytokines, chemokines, and
pathogen-derived products. Most studies attempting to identify the
mechanisms of hematopoiesis have focused on bacterial and viral
infections. From intracellular protozoan infections to large
multicellular worms, parasites are a global health burden and represent
major immunological challenges that remain poorly defined in the context
of hematopoiesis. Immune responses to parasites vary drastically, and
parasites have developed sophisticated immunomodulatory mechanisms that
allow development of chronic infections. Recent advances in imaging,
genomic sequencing and mouse models have shed new light on how parasites
induce unique forms of emergency hematopoiesis. In addition, parasites
can modify the hematopoiesis in the BM and periphery to improve their
survival in the host. Parasites can also induce long-lasting
modifications to HSCs, altering future immune responses to infection,
inflammation or transplantation, a term sometimes referred to as central
trained immunity. In this review, we highlight the current understanding
of parasite-induced hematopoiesis and how parasites target this process
to promote chronic infections.%
\end{abstract}%



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