Cell Signaling Technology

Product Pathways - Lymphocyte Signaling

CTLA-4 (D4E9I) Rabbit mAb #15119

CD278   CTLA-4   CTLA4   Cytotoxic T-lymphocyte protein 4  

No. Size Price
15119S 100 µl ( 200 tests ) ¥3,100.00 现货查询 购买询价
15119 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
F 1:200 Human, Endogenous 30 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: F=Flow Cytometry,

Specificity / Sensitivity

CTLA-4 (D4E9I) Rabbit mAb recognizes endogenous levels of total CTLA-4 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp100 of human CTLA-4 protein.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of human peripheral blood mononuclear cells, untreated (left) or PHA-treated (1 ug/ml, 72 hr; right), using CTLA-4 (D4E9I) Rabbit mAb and co-stained with a CD3 antibody. Anti-rabbit IgG (H+L), F(ab')2 Fragment (Alexa Fluor® 647 Conjugate) #4414 was used as a secondary antibody. Analysis was performed on cells in the lymphocyte gate.

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 down regulation 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).

  1. Brunet, J.F. et al. (1987) Nature 328, 267-70.
  2. Brunet, J.F. et al. (1988) Immunol Rev 103, 21-36.
  3. Dariavach, P. et al. (1988) Eur J Immunol 18, 1901-5.
  4. Linsley, P.S. (1995) J Exp Med 182, 289-92.
  5. Collins, A.V. et al. (2002) Immunity 17, 201-10.
  6. Rudd, C.E. et al. (2009) Immunol Rev 229, 12-26.
  7. Waterhouse, P. et al. (1995) Science 270, 985-8.
  8. Romo-Tena, J. et al. (2013) Autoimmun Rev 12, 1171-6.
  9. Wang, J. et al. (2014) PLoS One 9, e85982.
  10. Egen, J.G. et al. (2002) Nat Immunol 3, 611-8.
  11. Hodi, F.S. et al. (2003) Proc Natl Acad Sci U S A 100, 4712-7.
  12. Pardoll, D.M. (2012) Nat Rev Cancer 12, 252-64.

Application References

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Protocols


For Research Use Only. Not For Use In Diagnostic Procedures.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

Alexa Fluor is a registered trademark of Life Technologies Corporation.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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