The Soluble Isoform of CTLA-4 Correlates with Interferon-α Activity in Systemic Lupus Erythematosus

Lekh N Dahal, Robert N Barker, Frank J Ward*

*Corresponding author for this work

Research output: Contribution to journalLetter

Abstract

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder characterized by fluctuating levels of immune response hyperactivity, high serum titers of nucleic antigen-specific autoantibodies, and persistent production of type-I interferon (IFN)1 One route to controlling SLE has been to exploit the properties of T cell lymphocyte costimulation inhibitor (CTLA-4), a selective costimulation inhibitor, which suppresses autoantigen-specific T cell response intensity2.

Original languageEnglish
Article number190678
Number of pages4
JournalJournal of Rheumatology
DOIs
Publication statusE-pub ahead of print - 1 Dec 2019

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Systemic Lupus Erythematosus
Interferons
Protein Isoforms
T-Lymphocytes
Interferon Type I
Autoantigens
Autoantibodies
Lymphocytes
Antigens
Serum

Cite this

The Soluble Isoform of CTLA-4 Correlates with Interferon-α Activity in Systemic Lupus Erythematosus. / Dahal, Lekh N; Barker, Robert N; Ward, Frank J.

In: Journal of Rheumatology, 01.12.2019.

Research output: Contribution to journalLetter

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title = "The Soluble Isoform of CTLA-4 Correlates with Interferon-α Activity in Systemic Lupus Erythematosus",
abstract = "Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder characterized by fluctuating levels of immune response hyperactivity, high serum titers of nucleic antigen-specific autoantibodies, and persistent production of type-I interferon (IFN)1 One route to controlling SLE has been to exploit the properties of T cell lymphocyte costimulation inhibitor (CTLA-4), a selective costimulation inhibitor, which suppresses autoantigen-specific T cell response intensity2.",
author = "Dahal, {Lekh N} and Barker, {Robert N} and Ward, {Frank J}",
note = "ACKNOWLEDGMENT We are grateful to Dr. Nick Fluck, Dr. Neil Basu, Dr. Lars P Erwig, and Dr. Hazem Youssef for their invaluable support in recruiting patients for the study; Prof. Georgina L. Hold for assistance and interpretation with SNP studies; and Vivien Vaughan for her expertise in recruiting study participants and maintaining ethical documentation. This work was supported by Arthritis Research UK (Grant no. 19282). F.J. Ward, L.N. Dahal, and R.N. Barker have filed a patent covering the use of the monoclonal antibody targeting the soluble isoform of CTLA-4 as a therapeutic agent. L.N. Dahal and F.J. Ward share joint senior authorship of this article.",
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AU - Barker, Robert N

AU - Ward, Frank J

N1 - ACKNOWLEDGMENT We are grateful to Dr. Nick Fluck, Dr. Neil Basu, Dr. Lars P Erwig, and Dr. Hazem Youssef for their invaluable support in recruiting patients for the study; Prof. Georgina L. Hold for assistance and interpretation with SNP studies; and Vivien Vaughan for her expertise in recruiting study participants and maintaining ethical documentation. This work was supported by Arthritis Research UK (Grant no. 19282). F.J. Ward, L.N. Dahal, and R.N. Barker have filed a patent covering the use of the monoclonal antibody targeting the soluble isoform of CTLA-4 as a therapeutic agent. L.N. Dahal and F.J. Ward share joint senior authorship of this article.

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N2 - Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder characterized by fluctuating levels of immune response hyperactivity, high serum titers of nucleic antigen-specific autoantibodies, and persistent production of type-I interferon (IFN)1 One route to controlling SLE has been to exploit the properties of T cell lymphocyte costimulation inhibitor (CTLA-4), a selective costimulation inhibitor, which suppresses autoantigen-specific T cell response intensity2.

AB - Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder characterized by fluctuating levels of immune response hyperactivity, high serum titers of nucleic antigen-specific autoantibodies, and persistent production of type-I interferon (IFN)1 One route to controlling SLE has been to exploit the properties of T cell lymphocyte costimulation inhibitor (CTLA-4), a selective costimulation inhibitor, which suppresses autoantigen-specific T cell response intensity2.

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