Regulation of CTLA-4 recycling by LRBA and Rab11.


Journal

Immunology
ISSN: 1365-2567
Titre abrégé: Immunology
Pays: England
ID NLM: 0374672

Informations de publication

Date de publication:
09 2021
Historique:
revised: 30 03 2021
received: 01 03 2021
accepted: 13 04 2021
pubmed: 8 5 2021
medline: 6 10 2021
entrez: 7 5 2021
Statut: ppublish

Résumé

CTLA-4 is an essential regulator of T-cell immune responses whose intracellular trafficking is a hallmark of its expression. Defects in CTLA-4 trafficking due to LRBA deficiency cause profound autoimmunity in humans. CTLA-4 rapidly internalizes via a clathrin-dependent pathway followed by poorly characterized recycling and degradation fates. Here, we explore the impact of manipulating Rab GTPases and LRBA on CTLA-4 expression to determine how these proteins affect CTLA-4 trafficking. We observe that CTLA-4 is distributed across several compartments marked by Rab5, Rab7 and Rab11 in both HeLa and Jurkat cells. Dominant negative (DN) inhibition of Rab5 resulted in increased surface CTLA-4 expression and reduced internalization and degradation. We also observed that constitutively active (CA) Rab11 increased, whereas DN Rab11 decreased CTLA-4 surface expression via an impact on CTLA-4 recycling, indicating CTLA-4 shares similarities with other recycling receptors such as EGFR. Additionally, we studied the impact of manipulating both LRBA and Rab11 on CTLA-4 trafficking. In Jurkat cells, LRBA deficiency was associated with markedly impaired CTLA-4 recycling and increased degradation that could not be corrected by expressing CA Rab11. Moreover LRBA deficiency reduced CTLA-4 colocalization with Rab11, suggesting that LRBA is upstream of Rab11. These results show that LRBA is required for effective CTLA-4 recycling by delivering CTLA-4 to Rab11 recycling compartments, and in its absence, CTLA-4 fails to recycle and undergoes degradation.

Identifiants

pubmed: 33960403
doi: 10.1111/imm.13343
pmc: PMC8358724
mid: EMS126082
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
CTLA-4 Antigen 0
Clathrin 0
LRBA protein, human EC 2.7.10.-
rab11 protein EC 3.6.1.-
rab GTP-Binding Proteins EC 3.6.5.2
rab5 GTP-Binding Proteins EC 3.6.5.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

106-119

Subventions

Organisme : Wellcome Trust Clinical PhD Studentship
ID : 110297/Z/15/Z
Organisme : Wellcome Trust
ID : 204798
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/H013598/2
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 20478/Z/16
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/M503290/1
Pays : United Kingdom
Organisme : Versus Arthritis
ID : 21147
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/M009203/1
Pays : United Kingdom

Informations de copyright

© 2021 The Authors. Immunology published by John Wiley & Sons Ltd.

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Auteurs

Daniel Janman (D)

Institute of Immunity and Transplantation, University College London, London, UK.

Claudia Hinze (C)

Institute of Immunity and Transplantation, University College London, London, UK.

Alan Kennedy (A)

Institute of Immunity and Transplantation, University College London, London, UK.

Neil Halliday (N)

Institute of Immunity and Transplantation, University College London, London, UK.

Erin Waters (E)

Institute of Immunity and Transplantation, University College London, London, UK.

Cayman Williams (C)

Institute of Immunity and Transplantation, University College London, London, UK.

Behzad Rowshanravan (B)

Institute of Immunity and Transplantation, University College London, London, UK.

Tie Zheng Hou (TZ)

Institute of Immunity and Transplantation, University College London, London, UK.

Shane Minogue (S)

Institute of Liver and Digestive Health, University College London, London, UK.

Omar S Qureshi (OS)

Celentyx Ltd., Birmingham, UK.

David M Sansom (DM)

Institute of Immunity and Transplantation, University College London, London, UK.

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Classifications MeSH