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CTLA4 is a member of the immunoglobulin superfamily and encodes a protein which transmits an inhibitory signal to T cells. Zusätzlich bieten wir Ihnen CTLA4 Antikörper (455) und CTLA4 Proteine (82) und viele weitere Produktgruppen zu diesem Protein an.
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Data show that CTLA-4(+)PD-1 (zeige PDCD1 ELISA Kits)(-) memory CD4 (zeige 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 (zeige GUSB ELISA Kits), and contained replication-competent and infectious virus.
The potential of the CTLA4 and G250 co-expression DNA vaccine.
Tregs were observed to regulate CD4 (zeige CD4 ELISA Kits)(+), but not CD8 (zeige CD8A ELISA Kits)(+), T cell infiltration into tumors through a CTLA-4/CD80 (zeige CD80 ELISA Kits) dependent mechanism. Disrupting CTLA-4 interaction with CD80 (zeige CD80 ELISA Kits) was sufficient to induce CD4 (zeige CD4 ELISA Kits) T cell infiltration into tumors.
These results suggest that CD44 (zeige 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 (zeige 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 (zeige 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 (zeige 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 (zeige CD80 ELISA Kits)/CD86 (zeige 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 (zeige MLXIP ELISA Kits)-155 is modulated by a major dust mite allergen, Dermatophagoides farinae (Df1), and increases CD4 (zeige 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.
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 (zeige PDCD1 ELISA Kits) decreased in CD8 (zeige 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.
In children with idiopathic nephrotic syndrome (INS (zeige INS ELISA Kits)), serum CTLA-4 concentration significantly increased at remission compared with onset. Furthermore, a positive significant correlation was observed between Treg number and serum CTLA-4 level. This suggests that Treg and CTLA-4 are involved in the induction of remission in INS (zeige INS ELISA Kits).
The Genetic analysis of this study revealed that the very early onset JMG had a more prominent genetic predisposition in an immunomodulating gene (CTLA4).
Association between CTLA4 G allele/GG genotype and acute rejection risk in renal transplantation was found in this meta-analysis (G allele: OR=1.21, 95% CI: 1.03-1.44, P=.02; GG genotype: OR=1.37, 95% CI: 1.10-1.69, P=.004). However, the AA genotype was not associated with acute rejection risk in renal transplantation.
CTLA-4 polymorphisms are significant risk factors for transplant-related mortality and survival in children undergoing allogeneic hematopoietic stem cell transplantation and should be evaluated in further trials.
Review/Meta-analysis: CTLA4 +49A/G polymorphisms increased the risk of type 1 diabetes mellitus in children, and can be considered to be a genetic marker for T1D in children.
Suggest a truncated diphtheria toxin based recombinant porcine CTLA-4 fusion toxin as a novel approach for in vivo depletion of CD80 (zeige CD80 ELISA Kits)-positive cells.
The surface expression of CTLA-4 was increased in subclinical stages of paratuberculosis infection while levels of ZAP-70 (zeige ZAP70 ELISA Kits) were decreased in CD4 (zeige 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 (zeige 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 (zeige 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