|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||37682 Da|
|Other Names||T-lymphocyte activation antigen CD86, Activation B7-2 antigen, B70, BU63, CTLA-4 counter-receptor B72, FUN-1, CD86, CD86, CD28LG2|
|Target/Specificity||A synthetic peptide corresponding to residues near the N-terminus of human B7-2 was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||B7-2/CD86 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Receptor involved in the costimulatory signal essential for T-lymphocyte proliferation and interleukin-2 production, by binding CD28 or CTLA-4. May play a critical role in the early events of T-cell activation and costimulation of naive T-cells, such as deciding between immunity and anergy that is made by T- cells within 24 hours after activation. Isoform 2 interferes with the formation of CD86 clusters, and thus acts as a negative regulator of T-cell activation.|
|Cellular Location||Cell membrane; Single-pass type I membrane protein|
|Tissue Location||Expressed by activated B-lymphocytes and monocytes|
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Provided below are standard protocols that you may find useful for product applications.
B7-2 (CD86) is an important costimulatory molecule for the priming and activation of naive and memory T cells, respectively. Soluble CD86 is produced by resting monocytes and results from an alternatively spliced transcript (CD86deltaTM) characterized by deletion of the transmembrane domain (1). Engagement of CD28 with B7-1 and B7-2 ligands on antigen-presenting cells (APCs) provides a stimulatory signal for T-cell activation, whereas subsequent engagement of CTLA-4 with these same ligands results in attenuation of the response. Given their central function in immune modulation, CTLA-4- and CD28-associated signaling pathways are primary therapeutic targets for preventing autoimmune disease, graft versus host disease, graft rejection and promoting tumor immunity (2). It has also been shown that on B cells and macrophages, heat shock proteins GroES and GroEL both stimulated the expression of B7-2 (3)
1. Jeannin P, et al. Immunity 13(3):303-12, 2000.
2. Schwartz JC, et al. Nature 410(6828):604-8, 2001.
3. Galdiero M, et al. Int. J Immunopathol Pharmacol 18(4):637-44, 2005.
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