Creation of memory B cells and long-term immune response

The current climate of COVID-19 makes the topic of vaccines, antibodies and immune responses a daily conversation. Now, immunologists are not the only ones who want to know how our bodies respond to reinfection months, years, and sometimes decades after the first immune response. According to a new study by Tomohiro Kurosaki of Osaka University, this ability requires Bach2, a protein that regulates the expression of genes needed to direct selected activated B cells to become memory B cells. It is shown that there is.

Like most Biological process, The immune response is complex.They include many types cell And protein, perform an accurate step-by-step process. And most are still unknown. For example Memory B cells are a type of white blood cell that forms in the lymph nodes and spleen during infection. They persist for years, allowing a rapid and potent antibody-related response to reinfection by the same virus or bacterium. In contrast, plasma cells are much more abundant and help during initial infection by producing antibodies, but they can also be present in the body for extended periods of time. Kurosaki and his team focused their research on understanding why activated B cells, called germinal center B cells, become memory B cells. Plasma cells, Or will be recycled.

Scientists identify multiple types of B cells by the expression of markers (specific proteins). Based on specific markers, researchers identified a subset of B cells that they determined were prone to memory B cells. These are called professional memory B cells. They then examined mice lacking the protein Bach2, a transcription factor required for memory B cell production. These mice are known to be deficient in memory B cell production. Researchers have found that the lack of Bach2 is associated with a decrease in promemory B cells and an increase in the expression of a gene associated with a protein complex called mTORC1.

Further testing has shown the importance of mTORC1. “Finally, we found that mTORC1 signaling is less active in promemory B cells than in the final recycled cells,” says Kurosaki. We rescued Bach2 knockout mice by inhibiting mTORC1 activity (in other words, inducing a state of hypometabolism of mTORC1), allowing mice to produce memory B cells. Furthermore, in wild-type mice, artificially reducing the mTORC1 activity of B cells produced more memory B cells than normal, and increasing that activity had the opposite effect. However, the mTORC1 activity alone could not explain everything. Experiments have shown that a unique combination of Bach2 expression and reduced mTORC1 activity is required for memory B cells.

Understanding the process by which memory B cells are generated means that you can manipulate this process to benefit. “Given the importance of memory B cells in protecting us from reinfection, being able to induce their production may help develop efficient vaccines that will remain effective for years.” Mr. Kurosaki says.

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Efficient induction of immune cells that store antigens

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For more information:
Takeshi Inoue To emerge from the germinal center and become quiescent memory B cells, it depends on metabolic reprogramming and provision of survival signals. Experimental Medical Journal (2020). DOI: 10.1084 / jem.20200866

Provided by
Osaka University

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