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\begin{document}

\title{Skin Repair and Immunoregulatory Effects of Myeloid Suppressor Cells
from human cord blood on Atopic Dermatitis}



\author[1]{Seung-Min Hong}%
\author[1]{Chang-Hyun Kim}%
\author[1]{SUEON KIM}%
\author[1]{Jae-Ik Yoo}%
\author[1]{Soo-Hyun Jung}%
\author[2]{Chul Hwan Bang}%
\author[2]{Ji hyun Lee}%
\author[1]{Tai-Gyu Kim}%
\affil[1]{ViGenCell Inc}%
\affil[2]{Seoul St Mary's Hospital College of Medicine The Catholic University of Korea}%


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  \date{May 16, 2024}


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\begin{abstract}
\textbf{Background:} In our previous study, we achieved large-scale
expansion of bone marrow-derived suppressor cells (MDSCs) derived from
CD34+ cells cultured in human umbilical cord blood (hUCB) and
demonstrated the immunomodulatory properties of these cells. This study
aimed to assess the therapeutic efficacy of hUCB-MDSCs in the treatment
of atopic dermatitis (AD). \textbf{Methods:} \emph{Dermatophagoides
farinae} \textbf{(}Df)-induced NC/Nga mice (clinical score of 7) were
treated with hUCB-MDSCs or control drug. The mechanisms underlying the
therapeutic effects of hUCB-MDSCs were evaluated using dermatitis
scores, immunological parameters, skin histology, and skin barrier
function analysis. \textbf{Results:} hUCB-MDSCs demonstrated
immunosuppressive effects on both human and mouse CD4+ T cells.
hUCB-MDSC administration significantly reduced the clinical severity
scores and was associated with histopathological changes, such as
reduced inflammatory cellular infiltration, epidermal hyperplasia, and
fibrosis. hUCB-MDSC administration decreased the serum levels of IgE,
IL-4, IL-5, IL-13, IL-17, thymus- and activation-regulated chemokine
(TARC), and thymic stromal lymphopoietin (TSLP). Additionally,
hUCB-MDSCs altered the expression of skin barrier function-related
proteins such as filaggrin, involucrin, loricrin, and cytokeratin 10 and
suppressed Df restimulated T-cell activation through cell--cell
interactions. Furthermore, hUCB-MDSCs promote skin recovery and maintain
their therapeutic effect even after recurrence. \textbf{Conclusions:}
hUCB-MDSC administration improved Df-induced AD-like skin lesions and
led to the restoration of skin barrier function. Furthermore, hUCB-MDSC
treatment inhibited inflammatory responses and suppressed T-cell immune
function. Therefore, the results of this study support the potential for
hUCB-MDSCs as a novel treatment for AD.%
\end{abstract}%



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