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CTLA4 is a member of the immunoglobulin superfamily and encodes a protein which transmits an inhibitory signal to T cells. Additionally we are shipping CTLA4 Antibodies (453) and CTLA4 Proteins (83) and many more products for this protein.
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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.
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
CTLA-4 regulates atherosclerosis by suppressing proatherogenic immune responses.
Data suggest enhanced clinical benefit from combining CTLA-4 antigen blockade with poxvirus-based active immunotherapy.
These results indicate that CTLA-4 expression in the tumor environment of esophageal carcinoma is associated with poorer prognosis
Of several immunotherapies being investigated, antibodies that target the programmed cell death protein-1 (show PDCD1 ELISA Kits) (nivolumab and pembrolizumab) and cytotoxic T-lymphocyte antigen-4 (ipilimumab) immune checkpoint pathways are among the most promising for patients with Small cell lung cancer (SCLC), and are the focus of this review.
In oncology, the two main classes of Checkpoint inhibitors (CPI), which are the most advanced in clinical development are the anti-CTLA-4 and anti-PD-1 (show PDCD1 ELISA Kits)/PD-L1 (show CD274 ELISA Kits) antibodies (Abs). Three of these Abs have been approved by the FDA (show FDA ELISA Kits) for clinical use.CPI can have efficacy across several types of cancer.
No significant associations with RHD (show RHD ELISA Kits) were found for the IL1RN (show IL1RN ELISA Kits) rs447713 and CTLA4 rs3087243 SNPs.
Data show that interleukin-21 (show IL21 ELISA Kits)-primed cytotoxic T-cell lymphocytes (CTL) with cytotoxic T-lymphocyte associated protein 4 (CTLA-4) blockade is safe and produces durable clinical responses.
Analysis of copy number alterations identified a higher burden of copy number loss in nonresponders to CTLA-4 and PD-1 (show PDCD1 ELISA Kits) blockade and found that it was associated with decreased expression of genes in immune-related pathways.
the upregulation of others syncytial molecules, including LAG3 (show LAG3 ELISA Kits), CTLA4, CD28 (show CD28 ELISA Kits) and CD3 (show CD3 ELISA Kits), assisting the formation of syncytia with APC (show APC ELISA Kits) cells.
Our study reports a novel association of SNPs within CD86 (show CD86 ELISA Kits) and CTLA4 genes with pemphigus. The CD86 (show CD86 ELISA Kits) rs1129055 A allele appears to confer susceptibility to Pemphigus vulgaris (show DSG3 ELISA Kits) but not to pemphigus foliaceus (show DSG1 ELISA Kits).
nasopharyngeal carcinoma patients with high tumor CTLA-4 expression had a poorer prognosis than those with low expression.
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