Cytokines & Chemokines

Programmed death-ligand 1 (PD-L1) also known as cluster of differentiation 274 (CD274) or B7 homolog 1 (B7-H1), is a protein that in humans is encoded by the CD274 gene. PD-L1 is a 40 kDa type 1 transmembrane protein that has been speculated to play a major role in suppressing the immune system during particular events such as pregnancy, tissue allografts, autoimmune disease and other disease states such as hepatitis. Normally the immune system reacts to foreign antigens where there is some accumulation in the lymph nodes or spleen which triggers a proliferation of antigen-specific CD8+ T cell. The formation of PD-1 receptor / PD-L1 or B7.1 receptor /PD-L1 ligand complex transmits an inhibitory signal which reduces the proliferation of these CD8+ T cells at the lymph nodes and supplementary to that PD-1 is also able to control the accumulation of foreign antigen specific T cells in the lymph nodes through apoptosis which is further mediated by a lower regulation of the gene Bcl-2. PD-L

Programmed death-ligand 1 (PD-L1) also known as cluster of differentiation 274 (CD274) or B7 homolog 1 (B7-H1), is a protein that in humans is encoded by the CD274 gene. PD-L1 is a 40 kDa type 1 transmembrane protein that has been speculated to play a major role in suppressing the immune system during particular events such as pregnancy, tissue allografts, autoimmune disease and other disease states such as hepatitis. Normally the immune system reacts to foreign antigens where there is some accumulation in the lymph nodes or spleen which triggers a proliferation of antigen-specific CD8+ T cell. The formation of PD-1 receptor / PD-L1 or B7.1 receptor /PD-L1 ligand complex transmits an inhibitory signal which reduces the proliferation of these CD8+ T cells at the lymph nodes and supplementary to that PD-1 is also able to control the accumulation of foreign antigen specific T cells in the lymph nodes through apoptosis which is further mediated by a lower regulation of the gene Bcl-2. PD-L

Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic factor belonging to the TGF-beta super family and is necessary for neuron survival and phenotypic maintenance in the central and peripheral nervous systems. G-DNF has the potential to support the differentiation and survival of many neuron subpopulations, especially dopaminergic neurons and motor neurons, as well as Purkinje cells and sympathetic neurons. Sertoli cells, type 1 astrocytes, Schwann cells, neurons, pinealocytes and skeletal muscle cells are known to express GDNF in human. GDNF has been shown to interact with GFRA2 and GDNF family receptor alpha 1. Mutations in this gene may be associated with Hirschsprung's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS).The recombinant human G-DNF expressed in E.coli is a disulfide-linked homo-dimer, with an apparent molecular weight of 17 kDa.

Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic factor belonging to the TGF-beta super family and is necessary for neuron survival and phenotypic maintenance in the central and peripheral nervous systems. G-DNF has the potential to support the differentiation and survival of many neuron subpopulations, especially dopaminergic neurons and motor neurons, as well as Purkinje cells and sympathetic neurons. Sertoli cells, type 1 astrocytes, Schwann cells, neurons, pinealocytes and skeletal muscle cells are known to express GDNF in human. GDNF has been shown to interact with GFRA2 and GDNF family receptor alpha 1. Mutations in this gene may be associated with Hirschsprung's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS).The recombinant human G-DNF expressed in E.coli is a disulfide-linked homo-dimer, with an apparent molecular weight of 17 kDa.

Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic factor belonging to the TGF-beta super family and is necessary for neuron survival and phenotypic maintenance in the central and peripheral nervous systems. G-DNF has the potential to support the differentiation and survival of many neuron subpopulations, especially dopaminergic neurons and motor neurons, as well as Purkinje cells and sympathetic neurons. Sertoli cells, type 1 astrocytes, Schwann cells, neurons, pinealocytes and skeletal muscle cells are known to express GDNF in human. GDNF has been shown to interact with GFRA2 and GDNF family receptor alpha 1. Mutations in this gene may be associated with Hirschsprung's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS).The recombinant human G-DNF expressed in E.coli is a disulfide-linked homo-dimer, with an apparent molecular weight of 17 kDa.

CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) is also known as CD152, is an Inhibitory receptor acting as a major negative regulator of T-cell responses. CTLA-4 is a member of the immunoglobulin superfamily, which is expressed on the surface of T cells and transmits an inhibitory signal to T cells. CTLA-4 and CD28 are homologous receptors expressed by both CD4+ and CD8+ T cells, which mediate opposing functions in T-cell activation. Both receptors share a pair of ligands expressed on the surface of antigen-presenting cells (APCs). The affinity of CTLA-4 for its natural B7 family ligands, CD80 and CD86, is considerably stronger than the affinity of their cognate stimulatory co-receptor CD28.

CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) is also known as CD152, is an Inhibitory receptor acting as a major negative regulator of T-cell responses. CTLA-4 is a member of the immunoglobulin superfamily, which is expressed on the surface of T cells and transmits an inhibitory signal to T cells. CTLA-4 and CD28 are homologous receptors expressed by both CD4+ and CD8+ T cells, which mediate opposing functions in T-cell activation. Both receptors share a pair of ligands expressed on the surface of antigen-presenting cells (APCs). The affinity of CTLA-4 for its natural B7 family ligands, CD80 and CD86, is considerably stronger than the affinity of their cognate stimulatory co-receptor CD28.

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

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