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When antigens interact with antigen receptors on B cells, B cells activate and differentiate into antibody-producing cells (plasma cells)
TMDU researchers found that CD22 paradoxically enhances BCR signaling by interacting with cis-ligands and upregulating BCR expression to restore B-cell function in B-cell receptor (BCR) signaling defects
The rules of the children's game "Red Light, Green Light" are easy to follow: red always means stop, green always means forward
In a study published in Science Signaling in March, researchers from Tokyo Medical and Dental University (TMDU) revealed that CD22, a key molecule in B cell signaling, switches from an activated role when B cell receptor inhibitory (BCR) signaling Impairment is due to a genetic defect leading to immune dysregulation
Contact of the BCR with the foreign invader prompts B cells to produce antibodies, and CD22 inhibits BCR signaling to prevent the inappropriate release of antibodies by B cells
"CD45 normally enhances BCR signaling," explains Chizuru Akatsu, lead author of the study
To investigate the relationship between CD22 and the restoration of BCR signaling in the absence of CD45, the researchers disrupted the binding of all interacting partners of CD22, either continuously or briefly, and observed how this affected BCR signaling
"The results were completely unexpected," said senior author Takeshi Tsubata.
It turned out that the cells that restored the signal expressed abnormally high levels of BCR, which explains their ability to continue functioning relatively normally
"What's really interesting about this result is that it may provide a way to restore immune function in patients with immune disorders caused by a loss of B-cell signaling," Akatsu said
Given the presence of B cells and immunoglobulins - albeit in greatly reduced numbers - CD22 may be a useful therapeutic target in immunocompromised patients with defective BCR signaling
“The inhibitory coreceptor CD22 restores B cell signaling by developmentally regulating Cd45−/− immunodeficient B cells,” was published in Science Signaling at DOI: 10.
