I was a little confused on this point. Can an individual B cell change its own DNA, or is it rather that the higher mutation rate means that the set of B cells in the body can be considered as editing its own DNA?
The part of the immune system being described is the germinal center reaction. The 1 million times faster mutation rate only occurs for B-cells dividing in these structures and it's caused by some kind of chemical signaling (the name has slipped my mind). Importantly, it only effects the mutation rate of the thing that codes for the antibody the B-cell expresses, but it has been observed that in this part the mutation is pretty much random.
On average, by the way, there is about 1 point mutation in the part coding for antibodies for every single division in the germinal center. But since the particular mutation is random, I'm not sure I like describing this as the B-cell editing its own genome. It makes it more mysterious than necessary.
I should probably turn this part of my PhD thesis into a set of blog posts once I've defended..."affinity maturation" is a weird and wonderful process.
B cells also do something called Immunoglobulin class switching to change the structure of antibodies they produce when they encounter their antigen. Different types of antibodies interact with receptors on other cells in the immune system to facilitate the immune response.
Yup they splice and rejoin their DNA in specific sites as part of V(D)J recombination (this isn't the somatic hypermutation the article mainly focuses on, which is a B cell specific process). 'Our' gene editing tools (CRISPR) were not designed by us, but come from nature, so maybe not surprising!
