Publication

Pemphigus pathogenesis: Insights from light and electron microscopy studies

Sokol, E., 2016, [Groningen]: University of Groningen. 148 p.

Research output: ThesisThesis fully internal (DIV)

APA

Sokol, E. (2016). Pemphigus pathogenesis: Insights from light and electron microscopy studies. University of Groningen.

Author

Sokol, Ena. / Pemphigus pathogenesis : Insights from light and electron microscopy studies. [Groningen] : University of Groningen, 2016. 148 p.

Harvard

Sokol, E 2016, 'Pemphigus pathogenesis: Insights from light and electron microscopy studies', Doctor of Philosophy, University of Groningen, [Groningen].

Standard

Pemphigus pathogenesis : Insights from light and electron microscopy studies. / Sokol, Ena.

[Groningen] : University of Groningen, 2016. 148 p.

Research output: ThesisThesis fully internal (DIV)

Vancouver

Sokol E. Pemphigus pathogenesis: Insights from light and electron microscopy studies. [Groningen]: University of Groningen, 2016. 148 p.


BibTeX

@phdthesis{8af75cfa86b343329c166dd2edfdc55d,
title = "Pemphigus pathogenesis: Insights from light and electron microscopy studies",
abstract = "Pemphigus is a life-threatening autoimmune blistering disease caused by antibodies against proteins of desmosomes. Desmosomes are adhesion junctions that interconnect intermediate filament networks of neighboring cells. By targeting transmembrane proteins of desmosomes, desmoglein 1 (Dsg1) and desmoglein 3 (Dsg3), pemphigus autoantibodies induce their clustering and loss of cell-cell adhesion (acantholysis) in the epidermis of the skin and epithelium of the mucosal membranes, which results in blistering. How pemphigus autoantibodies induce blisters is the main research question of this thesis. Skin and mucosa taken from pemphigus patients were analyzed using large scale electron microscopy, named {\textquoteleft}{\textquoteright}nanotomy{\textquoteright}{\textquoteright} and novel findings are described. The datasets are open source available at www.nanotomy.org. Pemphigus skin was further investigated using an overlay of light and electron microscopy showing that desmoglein clusters are interdigitations between cells in which the amount of Dsg1 in desmosomes is reduced. Lastly antibodies from pemphigus patients were applied to cultured human skin cells, revealing redistribution of the targeted desmogleins in specific patterns. This thesis suggests that loss of cell-cell adhesion in pemphigus occurs due to the depletion of the targeted desmogleins which then cannot be incorporated into the desmosomes. If other desmoglein isoform are not expressed, desmosomes will {\textquoteleft}melt{\textquoteright} away resulting in loss of cell-cell adhesion.",
author = "Ena Sokol",
year = "2016",
language = "English",
isbn = "978-94-6259-982-6",
publisher = "University of Groningen",
school = "University of Groningen",

}

RIS

TY - THES

T1 - Pemphigus pathogenesis

T2 - Insights from light and electron microscopy studies

AU - Sokol, Ena

PY - 2016

Y1 - 2016

N2 - Pemphigus is a life-threatening autoimmune blistering disease caused by antibodies against proteins of desmosomes. Desmosomes are adhesion junctions that interconnect intermediate filament networks of neighboring cells. By targeting transmembrane proteins of desmosomes, desmoglein 1 (Dsg1) and desmoglein 3 (Dsg3), pemphigus autoantibodies induce their clustering and loss of cell-cell adhesion (acantholysis) in the epidermis of the skin and epithelium of the mucosal membranes, which results in blistering. How pemphigus autoantibodies induce blisters is the main research question of this thesis. Skin and mucosa taken from pemphigus patients were analyzed using large scale electron microscopy, named ‘’nanotomy’’ and novel findings are described. The datasets are open source available at www.nanotomy.org. Pemphigus skin was further investigated using an overlay of light and electron microscopy showing that desmoglein clusters are interdigitations between cells in which the amount of Dsg1 in desmosomes is reduced. Lastly antibodies from pemphigus patients were applied to cultured human skin cells, revealing redistribution of the targeted desmogleins in specific patterns. This thesis suggests that loss of cell-cell adhesion in pemphigus occurs due to the depletion of the targeted desmogleins which then cannot be incorporated into the desmosomes. If other desmoglein isoform are not expressed, desmosomes will ‘melt’ away resulting in loss of cell-cell adhesion.

AB - Pemphigus is a life-threatening autoimmune blistering disease caused by antibodies against proteins of desmosomes. Desmosomes are adhesion junctions that interconnect intermediate filament networks of neighboring cells. By targeting transmembrane proteins of desmosomes, desmoglein 1 (Dsg1) and desmoglein 3 (Dsg3), pemphigus autoantibodies induce their clustering and loss of cell-cell adhesion (acantholysis) in the epidermis of the skin and epithelium of the mucosal membranes, which results in blistering. How pemphigus autoantibodies induce blisters is the main research question of this thesis. Skin and mucosa taken from pemphigus patients were analyzed using large scale electron microscopy, named ‘’nanotomy’’ and novel findings are described. The datasets are open source available at www.nanotomy.org. Pemphigus skin was further investigated using an overlay of light and electron microscopy showing that desmoglein clusters are interdigitations between cells in which the amount of Dsg1 in desmosomes is reduced. Lastly antibodies from pemphigus patients were applied to cultured human skin cells, revealing redistribution of the targeted desmogleins in specific patterns. This thesis suggests that loss of cell-cell adhesion in pemphigus occurs due to the depletion of the targeted desmogleins which then cannot be incorporated into the desmosomes. If other desmoglein isoform are not expressed, desmosomes will ‘melt’ away resulting in loss of cell-cell adhesion.

M3 - Thesis fully internal (DIV)

SN - 978-94-6259-982-6

PB - University of Groningen

CY - [Groningen]

ER -

ID: 27459439