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Thesis

Sjögren’s disease autoantigen TRIM21/Ro52 is exposed during lytic cell death, facilitates immune complex formation and activates macrophages

Abstract:

Sjögren’s disease (SjD) causes localised inflammation of the lacrimal and salivary glands (SGs), and autoantibody production against ubiquitously expressed intracellular proteins such as TRIM21/Ro52 and TROVE2/Ro60. TRIM21 has vital intracellular roles, as an Fc receptor and E3 ubiquitin ligase. It binds antibody Fc domains on opsonised pathogens, which have escaped extracellular immunity and entered cytosols. TRIM21 ubiquitinates these pathogenic targets, driving their proteasomal degrada...

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Authors

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Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Oxford college:
University College
Role:
Author
ORCID:
0009-0009-1032-650X

Contributors

Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Supervisor
ORCID:
0000-0002-2619-1867
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Supervisor
ORCID:
0000-0001-6924-6402
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Supervisor
ORCID:
0000-0003-1441-1727


More from this funder
Funder identifier:
https://ror.org/052gg0110
Grant:
KENN 19 20 01
Programme:
Kennedy Trust Studentship, Kennedy Institute of Rheumatology, University of Oxford
More from this funder
Funder identifier:
https://ror.org/052gg0110
Programme:
Henni Mester Studentship, University College Oxford


DOI:
Type of award:
DPhil
Level of award:
Doctoral
Awarding institution:
University of Oxford


Language:
English
Keywords:
Subjects:
Pubs id:
2268925
Local pid:
pubs:2268925
Deposit date:
2025-07-24
ARK identifier:

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