The St. Jude researchers had previously shown that one of these cell types, marginal-zone B cells, can give rise to a cancer called mucosa-associated lymphoid tissue (MALT) lymphoma when the cells abnormally over-express a gene called Bcl10. The current finding suggests that a drug that blocks the action of Bcl10 could be an effective treatment for this cancer.
The researchers discovered that Bcl10 activates a pathway of molecular signals that drives antibody-producing B cells to mature into one of three different members of this family of immune system cells: follicular, marginal zone and B1 B cells. Mice lacking Bcl10 have a significant decrease in mature B cells and cannot launch an effective antibody response against bacteria in their bloodstream.
To learn how Bcl10 controls B cell development and function, the investigators studied mice in which the gene was inactivated. The mice produced nearly normal numbers of immature B cells. However, these cells did not mature normally. This showed that Bcl10 function is essential for B-cell development.
The researchers found that mice lacking a functional Bcl10 gene could not activate specific pathways of signaling molecules that belong to a family of proteins called NF-B. The NF-B proteins are normally activated by Bcl10 after B cells encounter invading organisms, such as bacteria. These proteins then cause B cells to fully mature and release antibodies targeted against those specific organisms.