B lymphocytes, the "B" of which comes from the fact that they are created in our "bone" marrow, are one of the most important immune cells in our bodies. One of the two major types of immune cells in the adaptive immune system, they play a critical role in the body's ability to fight off infection because they produce antibodies, which are a crucial component of the adaptive immune response to bacteria and viruses that successfully invade the body.
But B cells, like all the components of the immune system, must be kept in check because B cell activation initiates drastic physiological measures such as inflammation and cell killing. These actions are great for killing off unwanted bacteria and viruses, but they can also harm healthy human tissue. So over time humans and other mammals have evolved systems for ensuring that B cells are only activated and set loose when absolutely necessary.
For years, scientists have known that B cells have a self-regulatory mechanism that involves CD22 molecules on the cell surface, like a dampening switch that keeps B cells from becoming active. But scientists did not know how the molecule does so. Part of the problem was that they did not know the target of CD22.
Now that part of the mystery has been solved. According to a paper in an upcoming issue of the journal Nature Chemical Biology, the molecule CD22 targets itself.
This is a crucial first step in understanding the complete picture of how CD22 and B cell activation work, says James Paulson, Ph.D., who led the research with his colleagues in the Department o
Contact: Jason Bardi
Scripps Research Institute