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CTLA4 is a member of the immunoglobulin superfamily and encodes a protein which transmits an inhibitory signal to T cells.
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Data show that CTLA-4(+)PD-1 (show PDCD1 ELISA Kits)(-) memory CD4 (show CD4 ELISA Kits)(+) T cells, which share phenotypic markers with regulatory T cells, were enriched in SIV DNA in blood, lymph nodes (LN), spleen, and gut (show GUSB ELISA Kits), and contained replication-competent and infectious virus.
reveal a novel CTLA-4-mediated pathway to attenuate cytotoxic T-lymphocytes and indicate the importance of post-transcriptional mechanisms in the regulation of anti-tumor immune responses
The potential of the CTLA4 and G250 co-expression DNA vaccine.
Tregs were observed to regulate CD4 (show CD4 ELISA Kits)(+), but not CD8 (show CD8A ELISA Kits)(+), T cell infiltration into tumors through a CTLA-4/CD80 (show CD80 ELISA Kits) dependent mechanism. Disrupting CTLA-4 interaction with CD80 (show CD80 ELISA Kits) was sufficient to induce CD4 (show CD4 ELISA Kits) T cell infiltration into tumors.
These results suggest that CD44 (show CD44 ELISA Kits)(+)CD117(+) T cells are stem cells and a specific T-cell phenotype that initially develops in the thymus, but they do not progress through DN3 and DN4 stages, lack a DP stage, and potently suppress T-cell proliferation and modulate the CTLA-4 pathway.
data suggest that increased expression of checkpoint blockade molecules PD-1 (show PDCD1 ELISA Kits) and CTLA-4 on donor T cells is not sufficient to prevent GvHD, and that cooperation between checkpoint blockade signaling by host cells and donor Tregs is necessary to limit GvHD in allo-HSCT recipients
Treg cells expand in both humans and mice in blood-stage malaria and interfere with conventional T helper cell responses and follicular T helper (TFH)-B cell interactions in germinal centers. Mechanistically, Treg cells function in a critical temporal window to impede protective immunity through cytotoxic-T-lymphocyte-associated protein-4 (CTLA-4).
CTLA-4 expressed by FOXP3 (show FOXP3 ELISA Kits)(+) regulatory T cells prevents inflammatory tissue attack and not T-cell priming in arthritis.
results are consistent with a complex pathway in which CD28 (show CD28 ELISA Kits) is the primary driver of Treg proliferation and CTLA-4 functions as the main brake but is also dependent on TCR signals and interactions with CD80 (show CD80 ELISA Kits)/CD86 (show CD86 ELISA Kits)
CTLA-4(+) microvesicles can competitively bind B7 costimulatory molecules on bystander dendritic cells, resulting in downregulation of B7 surface expression.
this study shows that miR (show MLXIP ELISA Kits)-155 is modulated by a major dust mite allergen, Dermatophagoides farinae (Df1), and increases CD4 (show CD4 ELISA Kits)+ T cell proliferation through the downregulation of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) expression
Genetic polymorphisms of CTLA-4 gene on the nucleotide 49 at codon 17 of exon 1, TSHR gene SNP rs2268458 of intron 1, number of regulatory T cells and TRAb levels play a role as risk factors for relapse in patients with Graves' disease.
These results demonstrate that POSTN (show POSTN ELISA Kits) promotes the osteogenic differentiation of mesenchymal stem cells (MSCs) and that CTLA4 enhances the ectopic osteogenesis of MSCs-CTLA4-based tissue-engineered bone.
the polymorphism -318C/T of CTLA-4 gene is associated with RBC (show CACNA1C ELISA Kits) alloimmunization among sickle cell disease patients. This highlights the role played by CTLA-4 on post-transfusion alloantibody development
Meta-analysis found that CTLA4 -318C/T gene polymorphism is not associated with the risk of acute rejection in renal transplantation in overall populations.
Our goal was to stimulate antitumor immunity by combining SS1P or LMB-100 with anti-CTLA-4. We constructed a BALB/c breast cancer cell line expressing human mesothelin (show MSLN ELISA Kits) (66C14-M), which was implanted in one or two locations. SS1P or LMB-100 was injected directly into established tumors and anti-CTLA-4 administered i.p. In mice with two tumors, one tumor was injected with immunotoxin and the other was not.
Taken together, we found that Id3+ and CTLA-4+ endometrial cells were significantly higher in women with repeated implantation failure and recurrent miscarriage, suggesting the negative roles of these angiogenesis and immune tolerance markers involving in regulating endometrium receptivity.
Suggest that genetic polymorphisms of CTLA-4 function as sex-dependent risk factors for development of acute rejection in an Iranian kidney transplant population.
A phase Ib study of dasatinib plus ipilimumab in patients with gastrointestinal stromal tumor (GIST) and other sarcomas was performed on the basis of preclinical data demonstrating that combined KIT and CTLA-4 blockade is synergistic.
The data we presented here showed that CTLA-4 was highly expressed in regulatory T cells and PD-1 (show PDCD1 ELISA Kits) decreased in CD8 (show CD8A ELISA Kits)+ T cells in peripheral blood of SCLC patients, suggesting their unique mechanisms involved in immune regulation.
Significant differences in the CpG-methylation patterns between tumor tissues and matched controls were observed for CTLA4 showing a decreased methylation of this gene in non-small cell lung cancer patients. Expression studies confirmed that hypomethylation also resulted in increased expression of CTLA4.
Suggest a truncated diphtheria toxin based recombinant porcine CTLA-4 fusion toxin as a novel approach for in vivo depletion of CD80 (show CD80 ELISA Kits)-positive cells.
The surface expression of CTLA-4 was increased in subclinical stages of paratuberculosis infection while levels of ZAP-70 (show ZAP70 ELISA Kits) were decreased in CD4 (show CD4 ELISA Kits)+ T cells of both subclinical and clinical animals, indicating a change in T cell phenotype with disease state.
These results suggested that the expression level of CTLA-4 in CD4 (show CD4 ELISA Kits)-positive T cells has a potentially immunosuppressive function in bovine leukemia infection.
Experimental infection with bovine viral diarrhea virus did not provide evidence ofTreg activation based on expression of FoxP3 (show FOXP3 ELISA Kits) and CTLA4.
This gene is a member of the immunoglobulin superfamily and encodes a protein which transmits an inhibitory signal to T cells. The protein contains a V domain, a transmembrane domain, and a cytoplasmic tail. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. The membrane-bound isoform functions as a homodimer interconnected by a disulfide bond, while the soluble isoform functions as a monomer. Mutations in this gene have been associated with insulin-dependent diabetes mellitus, Graves disease, Hashimoto thyroiditis, celiac disease, systemic lupus erythematosus, thyroid-associated orbitopathy, and other autoimmune diseases.
cytotoxic T-lymphocyte-associated protein 4 precursor
, CD152 protein
, cytotoxic T-lymphocyte protein 4
, cytotoxic T-lymphocyte protein 4 isoform CTLA4-TM
, cytotoxic T-lymphocyte-associated protein 4
, costimulatory molecule B7 receptor
, cytotoxic T lymphocyte-associated antigen 4
, CD152 antigen
, cytotoxic T-lymphocyte-associated antigen 4
, CD152 isoform
, celiac disease 3
, cytotoxic T lymphocyte associated antigen 4 short spliced form
, cytotoxic T-lymphocyte antigen 4
, cytotoxic T-lymphocyte-associated serine esterase-4
, ligand and transmembrane spliced cytotoxic T lymphocyte associated antigen 4
, soluble form
, transmembrane form
, cytotoxic T lymphocyte-associated protein 4
, costimulatory molecule B7 receptor CD152