anti-Tumor Necrosis Factor Receptor Superfamily, Member 9 (TNFRSF9) Antibodies

Human Tumor Necrosis Factor Receptor Superfamily, Member 9 (TNFRSF9) interaction partners

1. structural and functional properties of both h4-1BB and h4-1BBL and reveals that covalent receptor dimerization amplifies h4-1BB signaling

2. 3 SNPs (rs161827, rs161818, and rs161810) of the CD137 gene and their association with ischemic stroke were studied in a northern Chinese Han population. rs161827 was significantly different between patients with and without diabetes and the controls. rs161818 and rs161810 differed significantly between patients without diabetes and the controls. All 3 were statistically significant in the combination stroke group.

3. Herein, we present LOAd703, a designed adenovirus armed with trimerized CD40L and 4-1BBL that activates the CD40 and 4-1BB pathways, respectively

4. Tonic 4-1BB costimulation in chimeric antigen receptors impedes T cell survival and is vector-dependent.

5. Cetuximab-mediated NK-cell expression of CD137 on tumor-infiltrating lymphocytes is dependent on FcgammaRIIIa polymorphism. In neoadjuvant cetuximab-treated patients with head and neck cancer, upregulation of CD137 by intratumoral, cetuximab-activated NK cells correlated with FcgammaRIIIa V/F polymorphism and predicted clinical response.

6. In this study we systematically evaluated a series of CAR constructs targeting glypican-3 (GPC3), which is selectively expressed on several solid tumors. We compared GPC3-specific CARs that encoded CD3zeta (Gz) alone or with costimulatory domains derived from CD28 (G28z), 4-1BB (GBBz), or CD28 and 4-1BB (G28BBz).

7. 4-1BB and 4-1BBL qualify as markers for prediction of patients' course and represent a valuable screening target for patients with acute myeloid leukemia at initial diagnosis.

8. the role of CD137-CRDI (cysteine rich domain I) in the binding of CD137-CD137L was further investigated.

9. Egr2-driven cell surface proteins LAG-3 and 4-1BB can identify dysfunctional tumor antigen-specific CD8(+) TIL.

10. Findings indicate that CD137 antigen is a useful marker that can be used for identifying Mycobacterium tuberculosis (Mtb)-reactive CD4(+) T cells (Mtb-reactive CD4(+) T cells) by flow cytometry.

11. Anti-4-1BB single chain variable fragments enhanced surface CD69 expression and interleukin-2 production in stimulated CCRF-CEM cells which confirmed the agonistic effect of the selected single chain variable fragments. The data from this study have provided a rationale for further experiments involving the biological functions of anti-4-1BB single chain variable fragments in future studies.

12. Studies suggest that adoptive T cell therapy and CD137 antigen offer much opportunity to raise the efficacy of current cancer immunotherapies.

13. Triple costimulation via CD80, 4-1BB, and CD83 ligand elicits the long-term growth of Vgamma9Vdelta2 T cells in low levels of IL-2.

14. in complex with T cell receptor, promotes memory T cells, cell respiration, fatty acid oxidation and mitochondrial biogenesis

15. These studies provide the first direct evidence that ligation of tumour necrosis factor superfamily members and their cognate receptors is important for the control of viral lytic replication.

16. Our findings provide a novel, TNFRSF9-positive, reactive astrocytic phenotype in human gliomas

17. Human genetic evidence for involvement of CD137 in atherosclerosis

18. As a result of becoming activated, transferred human T lymphocytes express the inducible surface antigens hPD-1 and hCD137 on their plasma membrane.

19. Our results provide biological explanations for the antitumor effects of CD19 CARs and for the observations that CD19 CAR T cells incorporating the 4-1BB costimulatory domain are more persistent than those incorporating CD28 in clinical trials.

20. upregulation of CD137 expression through LMP1 by EBV promotes cell survival in T or NK cells

Mouse (Murine) Tumor Necrosis Factor Receptor Superfamily, Member 9 (TNFRSF9) interaction partners

1. m4-1BBL and Gal-9 act together to aid aggregation of m4-1BB monomers to efficiently initiate m4-1BB signaling.

2. the CD137-CD137L pathway plays an important role in regulating VSMC phenotype transformation via activation of NFATc1 signaling pathway.

3. Tonic 4-1BB costimulation in chimeric antigen receptors impedes T cell survival and is vector-dependent.

4. fatty acid metabolism plays a crucial role in enhancing the cell cycle progression of anti-CD3-activated CD8(+) T cells in vitro and the anti-apoptotic effects of 4-1BB signaling on these cells.

5. CD137 signaling activates the pro-angiogenic Smad1/5 pathway, induces the phosphorylation of Smad1/5 and nuclear translocation of p-Smad1/5, which in turn promotes the expression and translocation of NFATc1. Blocking CD137 signaling with inhibitory anti-CD137 antibody could inhibit this activation and attenuated agonist anti-CD137 antibody-induced angiogenesis.

6. the role of CD137-CRDI (cysteine rich domain I) in the binding of CD137-CD137L was further investigated.

7. Data indicate that anti-CD137 agonists can function as inhibitors of CD137L signaling, resulting in the creation of tumor microenvironments unfavorable for tumor immune evasion.

8. These studies reveal that the costimulatory effects of TLR1-TLR2 signaling in CD8(+) T cells are in part mediated by 4-1BB and are important for mounting an effective antitumor immune response.

9. This study discovers the 4-1BB pathway signaling enhances inflammatory response and promotes pulmonary fibrosis induced by crystalline silica.

10. Constitutive interaction between 4-1BB and 4-1BBL on murine LPS-activated bone marrow dendritic cells masks detection of 4-1BBL by TKS-1 but not 19H3 antibody.

11. results indicate that one important diabetogenic function of CD137 is to promote the expansion and accumulation of beta cell-autoreactive CD8 T cells, and in the absence of CD137 or its interaction with CD137 ligand, type 1 diabetes progression is suppressed

12. High CD137 expression is associated with neoplasms.

13. Ly6C, 4-1BB, and KLRG1 have roles in the activation of lamina propria lymphocytes in the small intestine in a mouse model of Crohn's disease

14. CD137 Regulates NFATc1 Expression in Mouse VSMCs through TRAF6/NF-kappaB p65 Signaling Pathway.

15. 4-1BB triggering preferentially enhances the expansion of CD8+ T cells through the amplification of autocrine IL-2/IL-2R signaling loop.

16. c-IAP ubiquitin protein ligase activity is required for 4-1BB signaling and CD8(+) memory T-cell survival.

17. we conclude that in vivo 4-1BB signaling of myeloid cells negatively regulates peripheral T cell responses

18. activation of CD137 signaling decreases the stability of advanced atherosclerotic plaques via its combined effects on Teff cells, vascular smooth muscle cells, and macrophages

19. 4-1BB mediates the inflammatory responses in obese skeletal muscle by interacting with its ligand 4-1BBL on macrophages.

20. CD137-CD137L interactions mediated via regulation of CyPA contribute to the progression of atherosclerosis.