Anti-Mouse CLEC9A (CD370) [Clone 7H11] – Purified in vivo GOLD™ Functional Grade

RBL-2H3 cells engineered to express mouse CLEC9A with an HA tag

This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.

Liquid

Functional grade preclinical antibodies are manufactured in an animal free facility using only in vitro protein free cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.

Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.

Research Use Only

2 – 8° C Wet Ice

n vivo CLEC9A blockade, n vivo Ag targeting to CLEC9A+ DCs, ELISA IF, IP

7H11 activity is directed against mouse CLEC9A (CD370), also known as DC, NK lectin group receptor-1 (DNGR-1).

CLEC9A: A Key Regulator of Dendritic Cell Cross-Presentation and Antitumor Immunity

CLEC9A is a C-type lectin receptor that plays roles in antiviral immune function and antitumor immune surveillance¹. CLEC9A is an endocytic receptor found on murine and human conventional dendritic cells (cDC) that is highly effective at extracting antigens from dead cells and presenting them to CD8+ T cells, leading to activation. CLEC9A-mediated signaling operates via the MHC class I pathway and CLEC9A is thought to be a pattern recognition receptor (PRRs) for damage-associated molecular patterns (DAMPs). The CLEC9A ectodomains of both mouse and human orthologs bind across multiple species and cell lines, with the exception of bacteria and yeast, to all dead nucleated cells as well as some nonnucleated cells including apoptotic mouse platelets and erythrocytes. Rather than triggering immediate immune activation, CLEC9A binds to the actin filaments of damaged or dead cells, activates Syk, diverts the damaged or dead cells into a recycling endosomal compartment, and ultimately promotes antigen cross-presentation. Mouse and human CLEC9A share 53% identity.

CLEC9A is a target of anti-cancer immunotherapy development and tumor vaccine delivery¹. Antigen-targeted CLEC9A can potentially break immune tolerance by inducing CD4+ and CD8+ T cell responses. Additionally, targeting CLEC9A allows for the specific delivery of antigens to cDC1s, thereby avoiding random off-target effects due to the activation of other immune cells.

7H11 was generated by immunizing Wistar rats with RBL-2H3 cells expressing mouse CLEC9A fused to an HA epitope². Splenocytes were fused to the Y3 rat myeloma cell line and hybridoma supernatants were screened based on their ability to bind to a CLEC9A chimeric protein that produces β-galactosidase when bound. Successfully bound supernatants were additionally assessed by flow cytometry against a chimeric CLEC9A protein fused to GFP.

CLEC9A is abundantly expressed on conventional dendritic (cDC) cells. In mice, expression is restricted to the following subsets: CD8α⁺ cDC1s and CD103⁺ cDC1s. Additionally, in mice, CLEC9A is predominantly expressed in spleen, lymph nodes, and thymus.

Ubiquitous preformed acid-labile protein associated ligand(s)

Cross present antigen to CTL

1 Hussain Z, Zhang Y, Qiu L, et al. NPJ Vaccines. 10(1):27. 2025.
2 Sancho D, Mourão-Sá D, Joffre OP, et al. J Clin Invest. 118(6):2098-2110. 2008.
3 Joffre OP, Sancho D, Zelenay S, et al. Eur J Immunol. 40(5):1255-1265. 2010.
4 Picco G, Beatson R, Taylor-Papadimitriou J, et al. Eur J Immunol. 44(7):1947-1955. 2014.
5 Snyder AG, Hubbard NW, Messmer MN, et al. Sci Immunol. 4(36):eaaw2004. 2019.