CTLA-4 (Ipilimumab Biosimilar) Human mAb #57924
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Human IgG1 kappa |
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Description
| Endotoxin | <0.1 EU/μg of antibody |
Product Usage Information
Formulation
Storage
Specificity / Sensitivity
CTLA-4 (Ipilimumab Biosimilar) Human mAb was confirmed to bind to its intended target protein CTLA-4 using flow cytometry.
Species Reactivity:
Human
Source / Purification
CTLA-4 (Ipilimumab Biosimilar) Human mAb is produced at Cell Signaling Technology. Ipilimumab is an antibody directed against the extracellular region of human CTLA-4.
Background
Cytotoxic T-lymphocyte protein 4 (CTLA-4, CD152) is an Ig superfamily member that negatively regulates early T cell activation (1-4). The CTLA-4 protein is primarily expressed on T cells, including CD8+ cytotoxic T cells, CD4+ helper T cells, and CD4+/FoxP3+ regulatory T cells (1,2). CTLA-4 protein competes with CD28 for B7.1 (CD80) and B7.2 (CD86) binding at the cell surface, which results in the downregulation of T cell activity (5). The activation of SHP-2 and PP2A downstream of CTLA-4 attenuates TCR signaling (6). Research studies indicate that CTLA4 knockout mice display lymphoproliferative disorders leading to early death, confirming the role of CTLA-4 as a negative regulator of T cells (7). Mutations in the corresponding CTLA4 gene are associated with multiple disorders, including insulin-dependent diabetes mellitus, Graves' disease, Hashimoto thyroiditis, celiac disease, systemic lupus erythematosus, and type V autoimmune lymphoproliferative syndrome (8,9). Additional studies demonstrate that CTLA-4 blockade is an effective strategy for tumor immunotherapy (10-12).
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- Linsley, P.S. (1995) J Exp Med 182, 289-92.
- Collins, A.V. et al. (2002) Immunity 17, 201-10.
- Rudd, C.E. et al. (2009) Immunol Rev 229, 12-26.
- Waterhouse, P. et al. (1995) Science 270, 985-8.
- Romo-Tena, J. et al. (2013) Autoimmun Rev 12, 1171-6.
- Wang, J. et al. (2014) PLoS One 9, e85982.
- Egen, J.G. et al. (2002) Nat Immunol 3, 611-8.
- Hodi, F.S. et al. (2003) Proc Natl Acad Sci U S A 100, 4712-7.
- Pardoll, D.M. (2012) Nat Rev Cancer 12, 252-64.
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