Browse our CTLA4 Proteins (CTLA4)

Rhesus Monkey Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA4) interaction partners

1. Data show that CTLA-4(+)PD-1(-) memory CD4(+) T cells, which share phenotypic markers with regulatory T cells, were enriched in SIV DNA in blood, lymph nodes (LN), spleen, and gut, and contained replication-competent and infectious virus.

Mouse (Murine) Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA4) interaction partners

1. Endogenous Pdcd4 promotes immune response.

2. cancer vaccine formulation can dominantly determine synergy, or lack thereof, with CTLA-4 and PD-L1 checkpoint blockade therapy for cancer.

3. when CTLA-4 and PD-1 antibodies were combined with DCR-BCAT in MMTV-Wnt1 transgenic mice, a genetic model of spontaneous Wnt-driven tumors, complete regressions were achieved in the majority of treated subjects. These data support RNAi-mediated beta-catenin inhibition as an effective strategy to increase response rates to cancer immunotherapy.

4. show that Aire deficiency in mice expands the pool of CD4+ T cells capable of melanoma cell eradication and has additive effects with anti-CTLA-4 antibody in slowing melanoma tumor growth and increasing survival. Moreover, pharmacologic blockade of central T cell tolerance and peripheral checkpoint blockade in combination enhanced antimelanoma immunity in a synergistic manner

5. Anti-PD-1 and anti PDL-1 do not increase the formation of ADA, but anti-CTLA-4 and anti-OX-40 do increase the onset of ADA.

6. This study establishes the causality of CTLA4 insufficiency in gastric cancer and uncovers a role of type 2 inflammation in initiating gastric epithelial transformation.

7. Co-inhibiting the expressions of PD-1 and CTLA-4 can effectively suppress the growth of H22 hepatoma and promote the apoptosis of tumor cells in mice.

8. Immunogenic mouse neuroblastoma acquires adaptive immune resistance by up-regulating PD-L1 expression, whereas PD-L1 is of lesser consequence in nonimmunogenic neuroblastoma tumors. Combining PD-L1 checkpoint inhibition with whole tumor cell/anti-CTLA-4 vaccination enhanced tumor cell killing, cured mice with established tumors, and induced long-term immune memory (6 months).

9. the investigation of RANK and RANKL as possible novel immunotherapy targets in cancer is a rational approach. Here we have defined the mechanism of action of RANKL-RANK blockade in combination with anti-CTLA4, and provide insight into the combination efficacy observed in the case reports.

10. 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

11. The potential of the CTLA4 and G250 co-expression DNA vaccine.

12. Tregs were observed to regulate CD4(+), but not CD8(+), T cell infiltration into tumors through a CTLA-4/CD80 dependent mechanism. Disrupting CTLA-4 interaction with CD80 was sufficient to induce CD4 T cell infiltration into tumors.

13. These results suggest that CD44(+)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.

14. data suggest that increased expression of checkpoint blockade molecules PD-1 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

15. 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).

16. CTLA-4 expressed by FOXP3(+) regulatory T cells prevents inflammatory tissue attack and not T-cell priming in arthritis.

17. results are consistent with a complex pathway in which CD28 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/CD86

18. CTLA-4(+) microvesicles can competitively bind B7 costimulatory molecules on bystander dendritic cells, resulting in downregulation of B7 surface expression.

19. this study shows that miR-155 is modulated by a major dust mite allergen, Dermatophagoides farinae (Df1), and increases CD4+ T cell proliferation through the downregulation of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) expression

20. CTLA-4 regulates atherosclerosis by suppressing proatherogenic immune responses.

Human Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA4) interaction partners

1. This study demonstrates the deleterious effects of prior exposure to anti-CTLA4 on tumor-infiltrating lymphocytes Adoptive cell therapy response and shows that baseline IL9 levels can potentially serve as a predictive tool to select the appropriate sequence of immunotherapies.

2. our study provides the first evidence for CTLA-4 rs231775 as a prognostic variable for the survival of patients with sepsis and emphasizes the need for further research to reveal potential functional associations between CTLA-4 and the immune pathophysiology of sepsis.

3. CTLA-4 +49 G/A reached a GWAS significant association with Diabetes Mellitus, Type 1risk in Chinese Han population, affects CTLA-4 expression in Treg subsets and subsequently humoral immunity in T1D patients.

4. The expression of CTLA-4 was down-regulated in multiple sclerosis patients compared to controls.

5. The +49G allele confers susceptibility to hepatitis C virus infection and with male gender, both in chronic disease. In addition, the -319C/+49G haplotype confers susceptibility to hepatitis C virus genotype 3 infection. Our results support an important role of the -319 C/T and +49 A/G polymorphisms in hepatitis C virus infection

6. CTLA-4 Expression in CD4+ T Cells From Patients With LRBA Deficiency.

7. this study demonstrated that individuals with CTLA4 mutation had an increased susceptibility to Epstein-Barr virus infection

8. The expression of miR-155 increased in BD and associated with upregulation of TNF-alpha and downregulation of CTLA-4 genes.

9. The CTLA-4 rs3087243 G>A polymorphism increases susceptibility to Hepatocellular Carcinoma in an eastern Chinese Han population. CTLA-4 haplotypes may influence the development of Hepatocellular Carcinoma.

10. SNPs rs231775 and rs733618 were associated with higher risks of myasthenia gravis [meta-analysis]

11. cTFH cell dysregulation in patients with LRBA deficiency reflects impaired control of TFH cell differentiation because of profoundly decreased CTLA4 expression on regulatory T cells and probably contributes to autoimmunity in patients with this disease. Serial monitoring of cTFH cell frequencies is highly useful in gauging the clinical response of LRBA-deficient patients to CTLA4-Ig therapy.

12. Per-residue energy decomposition of the binding affinities of the two complexes revealed the unique fingerprint hot-spot sites in CTLA-4/B7-1 and CD28/B7-1 complexes

13. we provide protocols for isolation of human monocytes and their differentiation into dendritic cells (DC), purification of conventional and regulatory T-cell populations, and the assembly of CTLA-4-dependent Treg suppression assays.

14. This study suggests that CTLA-4 polymorphism rs231775 is relevant for relapse and survival after allogeneic HSCT in childhood and should be further investigated in clinical trials.

15. Interactions among CTLA4 and CD40 SNPs significantly increase the susceptibility to Grave's disease in Chinese patients.

16. These data indicated that CTLA-4 exon-1 49 A/G polymorphism may be associated with patient response to radionuclide (131) I therapy in Graves' disease.

17. The CTLA-4 polymorphism genotype distribution and allele frequencies were not significantly different between the NCGC patients and the control subjects in a Chinese Population

18. CTLA-4 may be required forT follicular regulatory cell differentiation and production and participates in intestinal damage caused by spontaneous autoimmunity.

19. Study confirmed substantial CTLA-4 expression and the localization of CTLA-4 in melanoma cell lines and tissues. Also, study found that CTLA-4 expressed by melanoma cells does not affect melanoma-specific cytotoxic T-lymphocytes in the effector phase.

20. CTLA-4 polymorphism at position 49 and CT60 may be potentially associated with the risk of GD among Saudi patients.

Pig (Porcine) Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA4) interaction partners

1. This research demonstrated that genetic variances in the CTLA4 gene had significant effects on Landrace piglet diarrhea resistance.

2. Suggest a truncated diphtheria toxin based recombinant porcine CTLA-4 fusion toxin as a novel approach for in vivo depletion of CD80-positive cells.

Cow (Bovine) Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA4) interaction partners

1. The surface expression of CTLA-4 was increased in subclinical stages of paratuberculosis infection while levels of ZAP-70 were decreased in CD4+ T cells of both subclinical and clinical animals, indicating a change in T cell phenotype with disease state.

2. These results suggested that the expression level of CTLA-4 in CD4-positive T cells has a potentially immunosuppressive function in bovine leukemia infection.

3. Experimental infection with bovine viral diarrhea virus did not provide evidence ofTreg activation based on expression of FoxP3 and CTLA4.