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CTLA-4 and T cell activation

Current Opinion in Immunology, 1999
The past year has seen significant advances in our understanding of the role of cytotoxic T lymphocyte antigen 4 (CTLA-4) in regulating T cell activation and tolerance. Recent studies indicate that CTLA-4 not only counterbalances CD28 signals but also can inhibit T cell responses independently of CD28. Recent work has also revealed a role for CTLA-4 in
M A, Oosterwegel   +4 more
openaire   +2 more sources

CTLA-4 directly inhibits osteoclast formation

Annals of the Rheumatic Diseases, 2008
CTLA-4 is a regulator of co-stimulation and inhibits the activation of T cells through interfering with the interaction of CD80/86 on antigen-presenting cells with CD28 on T cells. CTLA-4 binds to the surface of antigen-presenting cells, such as dendritic cells and monocytes through CD80/86.
R, Axmann   +8 more
openaire   +2 more sources

CTLA‐4 gene polymorphisms and natural soluble CTLA‐4 protein in psoriasis vulgaris

International Journal of Immunogenetics, 2006
SummaryCTLA‐4 molecule is an important inhibitor of T‐lymphocyte activation. Several single nucleotide polymorphisms (SNPs) in the CTLA‐4 gene were found, and their associations with many human diseases were described. So far, however, such studies have not been performed in psoriasis vulgaris in Caucasoids.
W, Luszczek   +9 more
openaire   +2 more sources

CTLA-4 AT-Repeat Polymorphism Reduces the Inhibitory Function of CTLA-4 in Graves' Disease

Thyroid, 2003
Graves' disease (GD) is thought to be an autoimmune disease with a strong genetic component. Candidate genes include human leukocyte antigen (HLA) class II genes and CTLA-4. The CTLA-4 gene has a variable length AT-repeat polymorphism in the 3'-untranslated region. We previously found that the AT-repeat of 104 bp or longer was associated with GD.
Masaki, Takara   +2 more
openaire   +2 more sources

Pituitary Expression of CTLA-4 Mediates Hypophysitis Secondary to Administration of CTLA-4 Blocking Antibody

Science Translational Medicine, 2014
CTLA-4 blocking antibody induces secondary hypophysitis by binding to CTLA-4 antigen and initiating a type II hypersensitivity reaction.
Shintaro, Iwama   +5 more
openaire   +2 more sources

Molecular and Cellular Functions of CTLA-4

2020
Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) is an inhibitory receptor belonging to the CD28 immunoglobulin subfamily, expressed primarily by T-cells. Its ligands, CD80 and CD86, are typically found on the surface of antigen-presenting cells and can either bind CD28 or CTLA-4, resulting in a costimulatory or a co-inhibitory response ...
Samya, Van Coillie   +2 more
openaire   +2 more sources

A Native Soluble Form of CTLA-4

Cellular Immunology, 2000
CTLA-4 is an immunoregulatory receptor expressed on the surface of activated T and B lymphocytes. The counterreceptors for CTLA-4 are the B7 family molecules. We describe alternatively spliced mRNAs expressed in hematolymphoid tissues of humans, mice, and rats that lack the transmembrane domain coded by exon 3 of the CTLA-4 gene.
Oaks, Martin   +5 more
openaire   +2 more sources

Anti-CTLA-4 Ab

2016
Ipilimumab (MDX-010, BMS-734016) is a fully human monoclonal immunoglobulin (IgG1) specific for human cytotoxic T lymphocyte-associated antigen 4 (CTLA-4, CD152), which is expressed on a subset of activated T cells as a negative regulator of T-cell activation.
openaire   +1 more source

Soluble CTLA-4 – A confounding factor in CTLA-4 based checkpoint immunotherapy in cancer

Immunology Letters
Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) is a receptor that inhibits the activity of T cells. The CTLA-4 gene consists of four different exons that enable four different isoforms of CTLA-4 to be generated through alternative splicing. Although sCTLA-4 might impede the therapeutic effect of anti-CTLA-4 treatments, the role of sCTLA-4 in the ...
Parviz Azimnasab-sorkhabi   +4 more
openaire   +2 more sources

Anti-CTLA-4 Monoclonal Antibodies

2011
The discovery of checkpoint proteins which regulate T cell activation and proliferation through inhibitory or stimulatory receptors has led to a new class of anti-tumor therapies. The goal of modulating these checkpoints is to overcome pathologic inhibition of T-cell activity which develops during tumorigenesis.
Arvin S. Yang, Jedd D. Wolchok
openaire   +1 more source

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