Anti-Mouse CD22 (Clone MB22-11) – Purified in vivo PLATINUM™ Functional Grade

Mouse CD22 cDNA-transfected baby hamster kidney cells

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 in vitro 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

MB22-11 activity is directed against mouse CD22 (Siglec-2).

Siglecs (sialic acid-binding immunoglobulin superfamily lectins) are a family of single pass, transmembrane cell surface proteins characterized by shared structural motifs and an ability to recognize sialic acids^{1, 2}. CD22 (Siglec-2), a 140 kDa member of the Siglec family expressed by B cells^{3, 4}, contains six C2-set domains, one V-set domain, and in its intracellular cytoplasmic tail has three immunoreceptor tyrosine-based inhibition motifs (ITIM) and one ITIM-like domain⁵. While murine Siglecs are not necessarily homologous to human Siglecs, CD22 is evolutionarily conserved and does have a direct human ortholog⁵.

CD22 acts as an inhibitory B cell co-receptor that negatively regulates B cell activation, B reg cell expansion, and B cell receptor (BCR) signaling⁴. Upon ligation of BCR, ITIMs are phosphorylated, leading to recruitment and activation of SH2-containing phosphatases that then dephosphorylate signaling molecules activated by BCR ligation⁴. Additionally, CD22 regulates B cell response to inflammation and is a master regulator of microglial phagocytosis in the aging brain⁵.

Evidence in mouse models suggests CD22 contributes to the pathogenesis of autoimmune diseases³. Loss of CD22 leads to hyperactivation of B cells⁵. CD22 mouse knockouts are defective in B cell development but do not develop lupus-like disease⁴.

To generate MB22-11, CD22 knockout mice were immunized with mouse CD22 cDNA-transfected baby hamster kidney cells⁶. Spleen cells were fused with NS-1 myeloma cells, and hybridomas producing antibody specifically reactive with CD22-transfected mouse L cells were selected and purified. MB22-11 was isotyped as IgG2c due to its C57BL/6 origin; however, both IgG2a and IgG2c specific reagents have significant reactivity against MB22-11.

In vitro, MB22-11 inhibits CD22-mediated adhesion by 90% and completely blocks CD22-Fc binding to T and B cells⁶. In vivo, MB22-11 significantly reduces peripheral blood, lymph node, and marginal zone B cell numbers^{6, 7}. Additionally, in mice injected with MB22-11, blood, spleen, and lymph node B cell turnover is higher relative to injection with non-blocking monoclonal antibodies, and B cell surface expression of CD22 is reduced to nearly undetectable levels⁶.

CD22 is expressed by most mature B cell lineages.

SHP-1, Syk, Lck, and Lyn

1. Bochner BS. Clin Exp Allergy. 39(3):317-324. 2009.
2. Kiwamoto T, Kawasaki N, Paulson JC, et al. Pharmacol Ther. 135(3):327-336. 2012.
3. Dörner T, Shock A, Smith KG. Int Rev Immunol. 31(5):363-378. 2012.
4. Tsubata T. Immunol Med. 42(3):108-116. 2019.
5. Siddiqui SS, Matar R, Merheb M, et al. Cells. 8(10):1125. 2019.
6. Haas KM, Sen S, Sanford IG, et al. J Immunol. 177(5):3063-3073. 2006.
7. Haas KM, Watanabe R, Matsushita T, et al. J Immunol. 184(9):4789-4800. 2010.