CAR T cells with dual targeting of CD19 and CD22 in pediatric and young adult patients with relapsed or refractory B cell acute lymphoblastic leukemia: a phase 1 trial.
up-regulation of siglec-2 in tumor tissues could predict better overall survival (OS) in hepatocellular carcinoma patients. Mechanisms of siglec-2 in hepatocellular carcinoma (HCC) development need further research.
CD22 plays a key role in affecting B cell responses to antigens and innate immune signals and CD22-CD22L interactions are essential for maintaining self-tolerance. The ability of CD22 to regulate both B cell receptor and toll-like receptors represents an attractive therapeutic strategy for manipulating B cell responses in autoimmunity.
Authors semi-quantitatively classified baseline expression of sCD19 and sCD22 in a large cohort of pediatric B-ALL. Dim CD19 and negative CD22 cases were correlated with common genetic abnormalities.
hCD22 transgenic mice develop normal humoral responses in a peanut allergy oral sensitization model. Homing of B cells to Peyer's patches was partially rescued by expression of hCD22 compared with CD22(-/-) B cells although not to wild-type levels.
Here the authors structurally characterize the ectodomain of CD22 and present its crystal structure with the bound therapeutic antibody epratuzumab which gives insights into the mechanism of inhibition of B-cell activation.
Conjugates of these multivalent ligands with auristatin and saporin toxins are efficiently internalized via hCD22 resulting in killing of B-cell lymphoma cells
This is the first time a NMR-based binding study of high affinity Siglec-2 (CD22) ligands in complex with whole Burkitt's lymphoma Daudi cells has been described.
We aimed to screen exons 9-14 of the CD22 gene which is a mutational hot spot region in B-precursor acute lymphoblastic leukemia (pre-B ALL) patients. Nine variants of which two novel were found. Novel variants were in introns 10 and 13. Gly745Asp (rs10406069) variant was missense and Cys790Arg (rs79438722) variant was silent.
results demonstrate that loss of high affinity CD22 ligands on GC B-cells occurs in both mice and humans through alternative mechanisms unmasking CD22 relative to naive and memory B-cells
Anti-CD22-magnetic nanoparticles-doxorubicin inhibited the proliferation of Raji cells significantly increased the uptake of doxorubicin and induced apoptosis.
These results suggest that the in vivo mechanism of non-ligand-blocking epratuzumab may in part involve the unmasking of CD22 to facilitate the trans-interaction of B cells with vascular endothelium.
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