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T cell immunoreceptor with Ig and ITIM domains (TIGIT) is an immune receptor present on some T cells and natural killer cells (NK). This protein could bind to CD155 (PVR) with high affinity, which causes increased secretion of IL-10 and decreased secretion of IL-12B and suppresses T-cell activation by promoting the generation of mature immunoregulatory dendritic cells. TIGIT could also bind to CD112 (PVRL2) with lower affinity. TIGIT’s inhibition of NK cytotoxicity can be blocked by antibodies against its interaction with PVR and the activity is directed through its ITIM domain.

T cell immunoreceptor with Ig and ITIM domains (TIGIT) is an immune receptor present on some T cells and natural killer cells (NK). This protein could bind to CD155 (PVR) with high affinity, which causes increased secretion of IL-10 and decreased secretion of IL-12B and suppresses T-cell activation by promoting the generation of mature immunoregulatory dendritic cells. TIGIT could also bind to CD112 (PVRL2) with lower affinity. TIGIT’s inhibition of NK cytotoxicity can be blocked by antibodies against its interaction with PVR and the activity is directed through its ITIM domain.

T cell immunoreceptor with Ig and ITIM domains (TIGIT) is an immune receptor present on some T cells and natural killer cells (NK). This protein could bind to CD155 (PVR) with high affinity, which causes increased secretion of IL-10 and decreased secretion of IL-12B and suppresses T-cell activation by promoting the generation of mature immunoregulatory dendritic cells. TIGIT could also bind to CD112 (PVRL2) with lower affinity. TIGIT’s inhibition of NK cytotoxicity can be blocked by antibodies against its interaction with PVR and the activity is directed through its ITIM domain.

T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-3 is an inhibitory molecule that is induced following T cell activation. TIM-3 is expressed by exhausted T cells in the settings of chronic infection and cancer, and tumor-infiltrating T cells that co-express PD-1 and TIM-3 exhibit the most severe exhausted phenotype. Tumor-infiltrating dendritic cells also express TIM-3. TIM-3 expression on DCs was found to suppress innate immunity by reducing the immunogenicity of nucleic acids released by dying tumor cells. Research studies show that heterodimerization of TIM-3 with CEACAM-1 is critical for the inhibitory function of TIM-3, and co-blockade of TIM-3 and CEACAM-1 enhanced antitumor responses in a mouse model of colorectal cancer. Its binding to Galectin-9 induces a range of immunosuppressive functions which enhance immune tolerance and inhibit anti-tumor immunity. TIM-3 ligation attenuates CD8+ and Th1 cell responses and promotes the activity of Treg and myeloid derived suppressor cells. In addition, dendritic cell-expressed TIM-3 dampens inflammation by enabling the phagocytosis of apoptotic cells and the cross-presentation of apoptotic cell antigens.

T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-3 is an inhibitory molecule that is induced following T cell activation. TIM-3 is expressed by exhausted T cells in the settings of chronic infection and cancer, and tumor-infiltrating T cells that co-express PD-1 and TIM-3 exhibit the most severe exhausted phenotype. Tumor-infiltrating dendritic cells also express TIM-3. TIM-3 expression on DCs was found to suppress innate immunity by reducing the immunogenicity of nucleic acids released by dying tumor cells. Research studies show that heterodimerization of TIM-3 with CEACAM-1 is critical for the inhibitory function of TIM-3, and co-blockade of TIM-3 and CEACAM-1 enhanced antitumor responses in a mouse model of colorectal cancer. Its binding to Galectin-9 induces a range of immunosuppressive functions which enhance immune tolerance and inhibit anti-tumor immunity. TIM-3 ligation attenuates CD8+ and Th1 cell responses and promotes the activity of Treg and myeloid derived suppressor cells. In addition, dendritic cell-expressed TIM-3 dampens inflammation by enabling the phagocytosis of apoptotic cells and the cross-presentation of apoptotic cell antigens.

TNF Receptor Type I, is also known as TNF R-p55/p60 and TNFRSF1A. It is a type I transmembrane protein member of the TNF receptor superfamily. It is expressed in most cell types. Binding of either TNF-α or TNF-β to TNF-R1 initiates a signal transduction pathway that results in the activation of the transcription factor NF-κB, whose target genes are involved in the regulation of inflammatory responses, and, in certain cells, induce apoptosis. TNF-R1 is essential for proper development of lymph node germinal centers and Peyer’s patches and for combating intracellular pathogens such as Listeria. It is stored in the Golgi and translocates to the cell surface following proinflammatory stimuli.

TNF Receptor Type I, is also known as TNF R-p55/p60 and TNFRSF1A. It is a type I transmembrane protein member of the TNF receptor superfamily. It is expressed in most cell types. Binding of either TNF-α or TNF-β to TNF-R1 initiates a signal transduction pathway that results in the activation of the transcription factor NF-κB, whose target genes are involved in the regulation of inflammatory responses, and, in certain cells, induce apoptosis. TNF-R1 is essential for proper development of lymph node germinal centers and Peyer’s patches and for combating intracellular pathogens such as Listeria. It is stored in the Golgi and translocates to the cell surface following proinflammatory stimuli.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseasesuch as Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseasesuch as Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseasesuch as Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-α) plays a major role in regulating growth, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells. In addition to inducing hemorrhagic necrosis of tumors, studies indicate TNF is involved in tumor igenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, Crohn’s disease, rheumatoid arthritis and graft-versus-host disease.

Tumor Necrosis Factor-Alpha (TNF-α) plays a major role in regulating growth, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells. In addition to inducing hemorrhagic necrosis of tumors, studies indicate TNF is involved in tumor igenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, Crohn’s disease, rheumatoid arthritis and graft-versus-host disease.

Tumor Necrosis Factor-Alpha (TNF-α) plays a major role in regulating growth, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells. In addition to inducing hemorrhagic necrosis of tumors, studies indicate TNF is involved in tumor igenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, Crohn’s disease, rheumatoid arthritis and graft-versus-host disease.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-alpha (TNF-a) is a homotrimer with a subunit molecular mass of 17.3 kDa. Tumor Necrosis Factor-alpha(TNF-a) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases; and in viral, bacterial, fungal, and parasitic infections. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease.

Tumor Necrosis Factor-alpha (TNF-a) is a homotrimer with a subunit molecular mass of 17.3 kDa. Tumor Necrosis Factor-alpha(TNF-a) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases; and in viral, bacterial, fungal, and parasitic infections. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease.

Tumor Necrosis Factor-alpha (TNF-a) is a homotrimer with a subunit molecular mass of 17.3 kDa. Tumor Necrosis Factor-alpha(TNF-a) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases; and in viral, bacterial, fungal, and parasitic infections. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.