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Journal article

The autoantigen TRIM21 assembles proinflammatory immune complexes after lytic cell death

Abstract:

Sjögren’s disease (SjD) causes localized and systemic inflammation and autoantibody production against intracellular proteins such as TRIM21/Ro52 (tripartite motif-containing protein 21). TRIM21, an E3 ubiquitin ligase, binds antibody Fc domains on opsonized pathogens that have escaped extracellular immunity and entered the cytosol. TRIM21 then ubiquitinates these pathogens, driving their proteasomal degradation. How TRIM21 becomes an autoantigen remains unclear. We show that TRIM21 is released upon lytic cell death (pyroptosis or necroptosis) but not apoptosis. Although many cytosolic proteins are released by dead cells, liberated TRIM21 is distinct: Its high antibody affinity enables binding to Fc domains of circulating immunoglobulins, forming large immune complexes (ICs). These ICs increase in SjD, where anti-TRIM21 autoantibodies interact with released TRIM21 via Fc and F(ab′)2. TRIM21 ICs are taken up by macrophages, which drive proinflammatory responses, antigen presentation, and metabolic changes in high interferon environments. Thus, TRIM21 may perpetuate inflammation and autoantigen presentation, resulting in high immunogenicity.

Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1126/sciimmunol.ads9680

Authors

More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
ORCID:
0000-0002-6145-6154
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
ORCID:
0009-0004-2423-591X


More from this funder
Funder identifier:
https://ror.org/03x94j517
Grant:
MR/W001217/1
More from this funder
Funder identifier:
https://ror.org/029chgv08
Grant:
224343/Z/21/Z
More from this funder
Grant:
KENN 20 21 12
KENN 21 22 02
KENN 19 20 01
More from this funder
Funder identifier:
https://ror.org/05ccjmp23


Publisher:
American Association for the Advancement of Science
Journal:
Science Immunology More from this journal
Volume:
11
Issue:
118
Article number:
eads9680
Publication date:
2026-04-17
Acceptance date:
2026-03-26
DOI:
EISSN:
2470-9468
Pmid:
41996473


Language:
English
Pubs id:
2395382
Local pid:
pubs:2395382
Deposit date:
2026-06-09
ARK identifier:

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