Gutenberg Open Science: Immunohistochemistry study in human orbital tissue of thyroid eye disease

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7263

Full metadata record

DC Field	Value	Language
dc.contributor.author	Hai, Yuanping	-
dc.date.accessioned	2022-07-07T12:19:57Z	-
dc.date.available	2022-07-07T12:19:57Z	-
dc.date.issued	2022	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/7277	-
dc.description.abstract	Thyroid eye disease (TED) is an orbital inflammatory disease. The current management is suboptimal because of unclear mechanisms. Many in vitro studies have confirmed that the pathogenesis involves several pathogenic pathways and a network of infiltrating mononuclear cells, cytokines, and chemokines in the orbit. However, the in vivo environment is sometimes different from the in vitro situation. Orbital tissue is the best sample to reflect local inflammation. Additionally, immunohistochemistry (IHC) analysis of orbital tissue can reveal the local orbital immunity and correlate the microscopic changes with the macroscopic clinical features. Several IHC studies have been performed in TED but with several limitations, and the pathogenesis of some molecules remains unclear. Uncovering the molecular mechanism that plays a significant role in TED may help develop novel therapeutic strategies and optimize the management of TED. In this study, we carried out staining of a large number of orbital tissue samples from patients with well-documented demographic and clinical data using antibodies against 18 proteins involved in multiple pathways that contribute to the pathogenesis of TED, and then investigated the primary mechanism. This study found that TSHR and IGF-1R signaling played a vital role in the pathogenesis of TED by activating pathways that resulted in the enhanced activation of orbital fibroblasts. T cells (CD3) and macrophages (CD68) were the main infiltrating immunocytes in the inflammatory stage of TED. IL-17A stimulated the differentiation of orbital fibroblasts into pre-adipocytes and myofibroblasts, and IL-17A, IL-23A, and IL-6 stimulated orbital fibroblasts to secrete hydrophilic hyaluronan and glycosaminoglycans. Furthermore, RANTES attracted T cells to migrate into the orbit, and MCP-1 promoted monocyte/macrophage migration into orbit. BAFF might participate in the primary mechanism by promoting B cell survival and maturation. The CD40-CD40L pathway is involved in the inflammatory response by mediating the interaction between orbital fibroblasts and T cells. Targeting these key players may provide more effective and disease-specific treatment strategies.	en_GB
dc.language.iso	eng	de
dc.rights	InCopyright	*
dc.rights.uri	http://rightsstatements.org/vocab/InC/1.0/	*
dc.subject.ddc	600 Technik	de_DE
dc.subject.ddc	600 Technology (Applied sciences)	en_GB
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	Immunohistochemistry study in human orbital tissue of thyroid eye disease	de_DE
dc.type	Dissertation	de
dc.identifier.urn	urn:nbn:de:hebis:77-openscience-854bcc80-7019-4866-802a-de88ba992df33	-
dc.identifier.doi	http://doi.org/10.25358/openscience-7263	-
jgu.type.dinitype	doctoralThesis	en_GB
jgu.type.version	Original work	de
jgu.type.resource	Text	de
jgu.date.accepted	2022-06-03	-
jgu.description.extent	VIII, 78 Seiten, Illustrationen, Diagramme	de
jgu.organisation.department	FB 09 Chemie, Pharmazie u. Geowissensch.	de
jgu.organisation.number	7950	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	600	de
jgu.subject.ddccode	610	de
jgu.organisation.ror	https://ror.org/023b0x485
Appears in collections:	JGU-Publikationen

Files in This Item:

	File	Description	Size	Format
	immunohistochemistry_study_in-20220630083423799.pdf		14.97 MB	Adobe PDF	View/Open

Show simple item record