Anti-CTLA-4 [9H10]

Catalogue Number: AB00894-22.0-BT-ABA

Manufacturer:Vector Laboratories, Inc (ABA)
Type:Recombinant Monoclonal
Alias:CD152; CTLA4; cytotoxic T-lymphocyte-associated antigen 4; Cytotoxic T-lymphocyte protein 4
Shipping Condition:Blue Ice
Unit(s): 1 mg
Host name: Armenian Hamster
Clone: 9H10
Isotype: IgG
Immunogen: This antibody was raised by immunising Syrian hamsters with Staphylococcus A bacteria coated in CTLA-4, isolating B cells from the immunised hamsters and fusing these with the P3X3.Ag8.653 myeloma line to produce stable hybridomas.
Application: ELISA, FC, WB, NT

Additional Text

Gene ID

12477

Gene Name

CTLA4

Uniprot ID

P09793

Purification

Purified

Antibody Clonality

Recombinant Monoclonal

Storage Note

Store at 4⁰C for up to 3 months. Note, this antibody is provided without added preservatives, it is therefore recommed this antibody be handled under sterile conditions. For longer storage, aliquot and store at -20⁰C.

Application Notes

CTLA-4 is upregulated on T cells following their activation, and acts as a negative regulator of T cell responses; CTLA-4 binds to the B7 molecules CD80 and 86, resulting in the delivery of an inhibitory signal, and consequent downregulation of T cell-mediated immunity. Administration of 9H10 blocks the interaction between CTLA-4 on the T cell surface and CD80 and CD86. This promotes the activation of effector T cells and stimulates the immune response raised against weak antigens, including tumour antigens. While this antibody alone does not enhance T cell proliferation, it does significantly increase T cell proliferation when administered together with anti-CD28 (clone 37.51) (Krummel & Allison, 1995), anti-OX40 and anti-GITR (Houot & Levy, 2009). Blocking CTLA-4 induces T cell anti-tumour immunity in animal models, both by suppressing regulatory T cell activity and directly promoting CD8+ T cell effector function (Peggs et al, 2009). In transgenic murine models of prostate cancer, the use of a CTLA-4 blockade in conjunction with an irradiated tumour cell vaccine stimulates an immune response against primary tumours, and results in a significant reduction in tumour incidence (Hurwitz et al, 2000). Similarly, in murine melanoma models, CTLA-4 blockage, in combination with CD40 stimulation and adenoviral vaccination, can elicit complete regression (Sorensen et al, 2010). In murine models of pancreatic ductal adenocarcinoma, 9H10 has also been shown to induce T cell-dependent tumour regressions (Vonderheide et al, 2015). Priming the T cell response with CD40 mAbs or chemotherapy reversed the resistance to 9H10 and RMP1-14 observed in well-established tumours. Additionally, this antibody has been used to detect CTLA-4 using ELISA (Krummel & Allison, 1995) and to stain CTLA-4-expressing cells (Deeths et al, 1999).