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The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Induction of autoimmune disease by deletion of CTLA-4 in mice in adulthood

Open access
Klocke, Katrin, Sakaguchi, Shimon, Holmdahl, Rikard, Wing, Kajsa·2016·Proceedings of the National Academy of Sciences

Abstract

Significance: Cytotoxic T lymphocyte antigen-4 (CTLA-4), up-regulated by activated conventional T cells and constitutively expressed by Foxp3+regulatory T cells, is essential for immunological self-tolerance. Because of early fatality in germ-line CTLA-4–deficient mice, the role in adulthood remains unclear. We abrogated CTLA-4 expression in adult mice and compared their phenotype with congenitally CTLA-4–deleted mice. We found that the two modes of CTLA-4 deficiency differed in resulting autoimmune disease phenotype and severity. Additionally, although CTLA-4–deficient mice had more severe collagen-induced arthritis, they were protected against peptide-induced experimental autoimmune encephalomyelitis (EAE). However, onset of protein-induced EAE was only delayed. These results taken together indicate that CTLA-4 deficiency affects both central and peripheral tolerance and Treg cell-mediated suppression.

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Metadata

Authors
Klocke, K., Sakaguchi, S., Holmdahl, R., & Wing, K.
Venue
Proceedings of the National Academy of Sciences
Published
2016-04-11
Volume
113
Issue
17
Pages
E2383-92
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2338484013
Cited by
232
References
9
FWCI
9.76
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Induction of autoimmune disease by deletion of CTLA-4 in mice in adulthood. https://app.cochat.ai/papers/10.1073/pnas.1603892113
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Klocke, K., Sakaguchi, S., Holmdahl, R., & Wing, K. (2016). Induction of autoimmune disease by deletion of CTLA-4 in mice in adulthood. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1603892113

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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