Publication: Glucocorticoid receptor modulates dendritic cell function in ulcerative colitis
Authors
Yang, Xinxin ; Geng, Jingshu
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/: 10.14670/HH-18-241
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info:eu-repo/semantics/article
Description
Abstract
Ulcerative colitis (UC) is a serious form of
inflammatory bowel disease (IBD) occurring worldwide.
Although anti-TNF therapy is found to be effective in
over 70% of patients with UC, nearly one-third are still
deprived of effective treatment. Because glucocorticoids
(GC) can effectively inhibit granulocyte-recruitment into
the mucosa, cytokine secretion and T cell activation,
they are used widely in the treatment of UC. However,
remission is observed in only 55% of the patients after
one year of steroid use due to a condition known as
steroid response. Additionally, it has been noted that
20%-40% of the patients with UC do not respond to GC
treatment. Researchers have revealed that the number of
dendritic cells (DCs) in patients with UC tends to
increase in the colonic mucosa. Many studies have
determined that the removal of peripheral DCs through
the adsorption and separation of granulocytes and
monocytes could improve tolerance of the intestine to its
symbiotic flora. Based on these results, further insights
regarding the beneficial effects of Adacolumn apheresis
in patients subjected to this treatment could be revealed.
GC can effectively inhibit the activation of DCs by
reducing the levels of major histocompatibility complex
class II (MHC II) molecules, which is critical for
controlling the recruitment of granulocytes. Therefore,
alternative biological and new individualized therapies
based on these approaches need to be evaluated to
counter UC. In this review, progress in research
associated with the regulatory effect of glucocorticoid
receptors on DCs under conditions of UC is discussed,
thus providing insights and identifying potential targets
which could be employed in the treatment strategies
against UC
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Citation
Histology and Histopathology Vol. 35, nĀŗ12 (2020)
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