United Kingdom (UK)
Recombinant monoclonal antibody to CD69. Manufactured using AbAb’s Recombinant Platform with variable regions (i.e. specificity) from the hybridoma 2.8.
UniProt Accession Number of Target Protein: Q07108
Alternative Name(s) of Target: AIM; BL-AC/P26; EA1; CLEC2C; GP32/28; MLR-3; Early activation antigen CD69; Activation inducer molecule; C-type lectin domain family 2 member C; Early T-cell activation antigen p60; Leukocyte surface antigen Leu-23
Immunogen: The original antibody was generated by fusing NS-1 myeloma cells with spleen cells from a CD69 (-/-) mouse that had previously been immunized 3 times with CD69 cells (pre-B 300-19 expressing the human CD69 molecule).
Specificity: This antibody binds human CD69. CD69 (cluster of differentiation 69), a membrane bound type II C-lectin disulfide–linked homodimer receptor, which is expressed on different leukocytes, including newly-activated lymphocytes, certain subtypes of memory T-cells, infiltrating lymphocytes isolated from patients with chronic inflammatory disorders, and regulatory T-cells. It is involved in lymphocyte proliferation and functions as a signal transmitting receptor in lymphocytes, natural killer (NK) cells, and platelets.
Application Notes: This antibody can be used for the analysis of CD69 expressed on the surface of cell surface using flow cytometry (PMID: 16983725). This antibody was used as a control antibody in in vivo mouse experiments as it does not bind mouse CD69 (PMID: 16983725; 27151919). This antibody was used in a study to show control on vaccinia virus (VACV) infection in both preventive and therapeutic treatment for transgenic mice expressing human CD69. Treatment in human-CD69 transgenic mouse model with the anti-huCD69-2.8 MAb could affect the primary adaptive response to VACV infection by increasing the number of activated T cells in the periphery (PMID: 31315995). In vivo CD69 targeting in mice expressing human CD69 induced rapid and massive mobilization of bone marrow leukocytes, which was inhibited by desensitization to S1P with FTY720. The treatment highly increased LSK and CLP cell proliferation and numbers, both in the periphery and in the bone marrow, and also augmented S1P1 and CXCR4 expression (PMID: 29483712).
Antibody first published in:
Esplugues et al. Enhanced antitumor immunity in mice deficient in CD69. J Exp Med. 2003 May 5;197(9):1093-106. PMID:12732655
Note on publication:
Describes the generation murine antibodies against mouse CD69 and evaluates their anti-tumor activity.