Trevigen Recombinant Par Biotin

Description: Mouse Monoclonal Human VEGI Antibody Biotin Conjugated, Flow Validated. Validated in WB and tested in Human.

Description: Mouse Monoclonal human CD3 Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Mouse Monoclonal human CD20 Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Mouse Monoclonal human CD10 Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Mouse Monoclonal human CD57 Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Mouse Monoclonal human HLA-DR Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Mouse Monoclonal human CD55/Daf Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Mouse Monoclonal human CD33/Siglec 3 Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Mouse Monoclonal human CD22/Siglec 2 Antibody Biotin Conjugated, Flow Validated. Validated in Flow Cytometry and tested in Human.

Description: Cell-mediated immune responses are initiated by T lymphocytes that are themselves stimulated by cognate peptides bound to MHC molecules on antigen-presenting cells (APC). T-cell activation is generally self-limited as activated T cells express receptors such as PD-1 (also known as PDCD-1) that mediate inhibitory signals from the APC. PD-1 can bind two different but related ligands, PDL-1 and PDL-2. Upon binding to either of these ligands, signals generated by PD-1 inhibit the activation of the immune response in the absence of "danger signals" such as LPS or other molecules associated with bacteria or other pathogens. Evidence for this is seen in PD-1-null mice who exhibit hyperactivated immune systems and autoimmune diseases. PD-1 is thus one of a growing number of immune checkpoint proteins.

Description: Cell-mediated immune responses are initiated by T lymphocytes that are themselves stimulated by cognate peptides bound to MHC molecules on antigen-presenting cells (APC). T-cell activation is generally self-limited as activated T cells express receptors such as PD-1 (also known as PDCD-1) that mediate inhibitory signals from the APC. PD-1 can bind two different but related ligands, PDL-1 and PDL-2. Upon binding to either of these ligands, signals generated by PD-1 inhibit the activation of the immune response in the absence of "danger signals" such as LPS or other molecules associated with bacteria or other pathogens. Evidence for this is seen in PD-1-null mice who exhibit hyperactivated immune systems and autoimmune diseases. PD-1 is thus one of a growing number of immune checkpoint proteins.

Description: PD-L1 Antibody: Cell-mediated immune responses are initiated by T lymphocytes that are themselves stimulated by cognate peptides bound to MHC molecules on antigen-presenting cells (APC) (1). T-cell activation is generally self-limited as activated T cells express receptors such as PD-1 (also known as PDCD-1) that mediate inhibitory signals from the APC (2). PD-1 can bind two different but related ligands, PD-L1 and PD-L2. PD-L1 is a B7-related protein that inhibits cell-mediated immune responses by reducing the secretion of IL-2 and IL-10 from memory T cells (3). This suggests that PD-L1 may be useful in reducing allogenic CD4+ memory T-cell responses to endothelial cells, thereby reducing the likelihood of host immune responses to allografts. PD-L1 also functions as an immune checkpoint protein, and multiple anti-PD-L1 antibodies are currently in phase II and III clinical trials, with one antibody already approved for the treatment of cancer (4).

Description: PD-L1 Antibody: Cell-mediated immune responses are initiated by T lymphocytes that are themselves stimulated by cognate peptides bound to MHC molecules on antigen-presenting cells (APC) (1). T-cell activation is generally self-limited as activated T cells express receptors such as PD-1 (also known as PDCD-1) that mediate inhibitory signals from the APC (2). PD-1 can bind two different but related ligands, PD-L1 and PD-L2. PD-L1 is a B7-related protein that inhibits cell-mediated immune responses by reducing the secretion of IL-2 and IL-10 from memory T cells (3). This suggests that PD-L1 may be useful in reducing allogenic CD4+ memory T-cell responses to endothelial cells, thereby reducing the likelihood of host immune responses to allografts. PD-L1 also functions as an immune checkpoint protein, and multiple anti-PD-L1 antibodies are currently in phase II and III clinical trials, with one antibody already approved for the treatment of cancer (4).

Description: TIGIT Antibody: The T cell immunoreceptor with Ig and ITIM domains (TIGIT) is a member of the PVR (poliovirus receptor) family of immunoglobin proteins. It is expressed on several classes of T cells including follicular B helper T cells (TFH). TIGIT has been shown to bind PVR with high affinity; this binding is thought to assist interactions between TFH and dendritic cells to regulate T cell dependent B cell responses (1). Similar to other immune checkpoint proteins such as PD-1, TIGIT is upregulated on exhausted T cells in chronic viral infections and cancer. Blockade of both TIGIT and PD-1 pathways leads to tumor rejection in mice suggesting that it may be of therapeutic use against cancer (2).

Description: TIGIT Antibody: The T cell immunoreceptor with Ig and ITIM domains (TIGIT) is a member of the PVR (poliovirus receptor) family of immunoglobin proteins. It is expressed on several classes of T cells including follicular B helper T cells (TFH). TIGIT has been shown to bind PVR with high affinity; this binding is thought to assist interactions between TFH and dendritic cells to regulate T cell dependent B cell responses (1). Similar to other immune checkpoint proteins such as PD-1, TIGIT is upregulated on exhausted T cells in chronic viral infections and cancer. Blockade of both TIGIT and PD-1 pathways leads to tumor rejection in mice suggesting that it may be of therapeutic use against cancer (2).

Description: The immune checkpoint protein TIM3 is a member of the immunoglobulin superfamily and TIM family of proteins that was initially identified as a specific marker of fully differentiated IFN-γ producing CD4 T helper 1 (Th1) and CD8 cytotoxic cells. It is a Th1-specific cell surface protein that regulates macrophage activation and negatively regulates Th1-mediated auto- and alloimmune responses, and is also highly expressed on regulatory T cells, monocytes, macrophages, and dendritic cells (1). TIM3 and PD-1 are co-expressed on most CD4 and CD8 T cells infiltrating solid tumors or in hematologic malignancy in mice; blocking TIM3 in conjugation with a PD-1 blockade increases the functionality of exhausted T cells and synergizes with to inhibit tumor growth (2,3).

Description: The immune checkpoint protein TIM3 is a member of the immunoglobulin superfamily and TIM family of proteins that was initially identified as a specific marker of fully differentiated IFN-γ producing CD4 T helper 1 (Th1) and CD8 cytotoxic cells. It is a Th1-specific cell surface protein that regulates macrophage activation and negatively regulates Th1-mediated auto- and alloimmune responses, and is also highly expressed on regulatory T cells, monocytes, macrophages, and dendritic cells (1). TIM3 and PD-1 are co-expressed on most CD4 and CD8 T cells infiltrating solid tumors or in hematologic malignancy in mice; blocking TIM3 in conjugation with a PD-1 blockade increases the functionality of exhausted T cells and synergizes with to inhibit tumor growth (2,3).