anti-Programmed Cell Death 1 (PDCD1) 抗体

Human Programmed Cell Death 1 (PDCD1) interaction partners

1. Increased FUT4 expression led to reduced OS in operable LUAD. FUT4 showed significant correlation with immune response and PD-1 expression

2. there were no statistically significant associations among the remaining 13 SNPs and the risk of intrauterine infection of HBV. The examination implied that hereditary variants of PDCD1 and LTA genes were associated with intrauterine infection of HBV.

3. These results provide support for the expression of PD-L1 in systemic mastocytosis and cutaneous mastocytosis, and PD-1 expression in CM.

4. PD-1 expression in breast tumor-infiltrating CD8-positive T cells.

5. Our results characterise the expression profiles of PD-1 and PD-L1proteins in head and neck squamous cell carcinoma which might serve as possible clinical prognostic markers

6. The frequency of PD1(+)CD8(+) T-cells may predict the prognosis of patients with gastric cancer.

7. The results that SNPs in PDCD! are associated with susceptibility to chronic autoimmune thrombocytopenia and lower response to predinisolone therapy.

8. This study aimed to evaluate whether PD1.1 (c.-606G>A), PD1 (c.627 + 252C>T), PD1.5 (c.804C>T), and PD1.9 (c.644C>T) single nucleotide polymorphisms of PDCD1 gene influence the risk, clinicopathological aspects, and survival of cutaneous melanoma.

9. HLA-G, NRP1, and PD-1, may be involved in the immune response in psoriatic patients

10. Proportions of naive CD4+ T cells were lower in young patients than in age-matched controls, and actually comparable to those in old patients and controls. This was accompanied with increased percentages of memory CD4+ T cells expressing HLA-DR, Ki-67, and PD-1 in young melanoma patients in comparison to the age-matched controls, but not in old patients.

11. This meta-analysis demonstrates the PD-1 rs36084323 A > G polymorphism is associated with decreased cancer risk in Asian

12. there is no significant association between PD1.3G/A - rs11568821 polymorphism and systemic lupus erythematosus or rheumatoid arthritis susceptibility in Southern Brazilian population.

13. SLC18A1 might complement other biomarkers currently under study in relation to programmed cell death protein 1/programmed cell death protein ligand 1 inhibition

14. Structural and functional analyses unexpectedly reveal an N-terminal loop outside the IgV domain of PD-1. This loop is not involved in recognition of PD-L1 but dominates binding to nivolumab, whereas N-glycosylation is not involved in binding at all.

15. This finding suggested the potential application of PD-1 blockade in AML. The present work demonstrated an excellent synergistic tumour therapeutic effect of PD-1 blockade and CTL therapy compared with either treatment alone.

16. High PD-1 expression is associated with Mycobacterium avium complex-induced lung disease.

17. PD-1/PD-L1 expression is a frequent occurrence in poorly differentiated neuroendocrine carcinomas of the digestive system.

18. Results indicated that high-level PD1 expression may be an important factor associated with the immune checkpoint pathway in liver cancer.

19. These results suggest that the PD-1 genotype of the donor plays an important role for the development of acute GvHD after alloHSCT from HLA-identical sibling donors.

20. We conclude that a subgroup of advanced disease ovarian cancer patients with high grade tumors, expressing PD-L1, may be prime candidates for immunotherapy targeting PD-1 signaling

Cow (Bovine) Programmed Cell Death 1 (PDCD1) interaction partners

1. Our findings confirm that PD-1 plays a vital role in peripheral blood lymphopenia and apoptosis caused by acute Bovine viral diarrhea virus infection, and provide new insights into exploring the immunopathological mechanisms of BVDV or other members of the Flaviviridae family, and a potential therapeutic strategy to control BVDV infection.

2. These results suggest that the PD-1/PD-L1 pathway could be involved in immune exhaustion of bovine mycoplasma-specific T cells. In conclusion, our study opens up a new perspective in the therapeutic strategy for bovine mycoplasmosis by targeting the immunoinhibitory receptor pathways.

3. PD-1 and LAG-3 cooperatively mediate the functional exhaustion of CD4(+) and CD8(+) T cells and are associated with the development of B-cell lymphoma in BLV-infected cattle.

4. M. bovis infection increased the expression of the PD-1 receptor on total PBMCs and in gated CD4(+) and CD8(+) T-cell subpopulations.

Mouse (Murine) Programmed Cell Death 1 (PDCD1) interaction partners

1. Our findings demonstrate that the modulation of T follicular helper cells by PD-1 signaling is dependent on the cytokines IL-10, IFN-gamma and MCP-1 in infection treatment vaccine-immunized mice.

2. Oncolytic herpes virotherapy and PD-1 blockade in a murine rhabdomyosarcoma model is an efficient treatment strategy.

3. These results show that PD-1 plays an inhibitory role during the naive-to-effector CD8 T cell transition and that the PD-1 pathway can also be modulated at this stage of T cell differentiation.

4. Blockade of CCR5-mediated myeloid derived suppressor cell accumulation enhances anti-PD1 efficacy in gastric cancer

5. T-cell activation mediates the immunopreventive effects of anti-PD-1; PD-1 on T cells interacts with the PD-1 ligand PD-L1 on cancer cells

6. these data show that PD-1 expression is an intrinsic property of brain-resident memory CD8 T cells in a persistent CNS viral infection

7. Our results demonstrate that entinostat enhances the antitumor effect of PD-1 targeting through functional inhibition of MDSCs and a transition away from an immune-suppressive tumor microenvironment. These data provide a mechanistic rationale for the clinical testing and potential markers of response of this novel combination in solid tumor patients.

8. synergism in cell death by Caspase-1- and RipK3 resulted in restriction of PD-1 and TIM3 expression on primed CD8(+) T cells, which promoted the survival of activated CD8(+) T cells.

9. Tim-3 and PD-1 pathways play critical roles in regulating CD8(+) T cell function and maintaining normal pregnancy.

10. Anti-PD-1/PD-L1 therapy inhibited CMT167 orthotopic lung tumors by 95%. .Silencing PD-L1 expression in CMT167 cells resulted in smaller orthotopic tumors that remained sensitive to anti-PD-L1 therapy, whereas implantation of CMT167 cells into PD-L1(-) mice blocked orthotopic tumor growth, indicating a role for PD-L1 in both the cancer cell and the microenvironment.

11. Combination therapies that depend on checkpoint inhibitor antibodies (Abs) such as for PD-1 or its ligand (PD-L1) together with immune stimulatory agonist Abs like anti-OX40 are being tested in the clinic to achieve improved antitumor effects

12. Inhibition of Fut8, a core fucosyltransferase, by genetic ablation or pharmacologic inhibition reduced cell-surface expression of PD-1 and enhanced T cell activation, leading to more efficient tumor eradication.

13. An examination of the mechanisms of immunity behind this long-term protection in PD-1 knockout mice showed a key role for parasite-specific CD8(+) T cells even when CD4(+) T cells and B cells responded to re-infection.

14. To test the in vivo activity of REGN2810, which does not cross-react with murine PD-1, knock-in mice were generated to express a hybrid protein containing the extracellular domain of human PD-1, and transmembrane and intracellular domains of mouse PD-1

15. The combination of tumor vaccination to induce high avidity tumor specific T cell responses and PD-1 blockade synergises to provide tumor therapy and 85% survival in the aggressive B16 melanoma model.

16. Blockade of PD-1 with monoclonal antibody may be an effective treatment during the postoperative period for restoring surgery-induced immunosuppression.

17. Data suggest that genetic or environmental factors that even moderately affect the expression of both PD-1 and FoxP3 can cause life-threatening autoimmune diseases by disrupting the T-cell homeostasis.

18. Data (including data from studies in transgenic/knockout mice) suggest that T-cell expression of Mirn155 is required to limit melanoma growth; miR-155, Pdcd1, Pdcd1l1, and Ctla4 appear to regulate overlapping pathways promoting antitumor immunity. [Mirn155 = microRNA 155; Pdcd1 = programmed cell death 1 protein; Pdcd1l1 = programmed cell death 1 ligand 1 protein; Ctla4 = cytotoxic T-lymphocyte-associated protein 4]

19. PD-1 plays a vital role in brain inflammation via regulation of Fgl-2 after ICH, and that manipulation of PD-1 might be a promising therapeutical target in ICH.

20. We identified PD-1 to be specifically expressed in PLZF(+) ILCp and revealed that the timing and order of expression of the transcription factors NFIL3, ID2, and TCF-1 was critical. Importantly, induction of ILC lineage commitment required only transient expression of NFIL3 prior to ID2 and TCF-1 expression.

Rhesus Monkey Programmed Cell Death 1 (PDCD1) 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.

2. Compared to before immunosuppression, PD-1 expression increased at reactivation. Increased T cells before zoster is likely due to virus reactivation.

3. A PD-1(high) phenotype is associated with accelerated in vivo CD8 T cell turnover in SIV-infections, especially within the SIV-specific CD8 T cell pool.

4. High levels of PD-1 expression on CD4(+) T cells in lymph nodes of rhesus macaques can serve as a valuable marker to identify T follicular helper cells.

5. Data indicate that PD-1 expression is increased as a result of T cell activation during a primary immune response as well as during persistent immune activation in macaques.

6. PD-1 can serve as a sensitive indicator of persistent, low-level virus replication