Maria, I commented on this subject in a different thread, but I know that navigating the forum can be challenging, particularly if the thread in question is more than a day old. So here goes:
B cells are a type of while blood cell, also called leukocytes. There are several different kinds of leukocytes: Neutrophils, Eosinophils, Basophils (these three are also called granulocytes, as they carry bits of protein used for a variety of immune system functions), Monocytes, and two forms of Lymphocytes: B cells and T cells, both of which are important players in Wegener’s and similar diseases. You won’t see anything labeled “B cells” in a normal blood panel, But you might see a breakdown of the various while blood cell components, including a line called “lymphocytes”, or “LY”, measured in both absolute numbers and as a percentage of total leukocytes. A differentiation of B cells from the various kinds of T cells takes more specialized tests, These are sometimes asked for, but rarely, unless there is a specific need. In the case of B cells, the measurement is an aid in telling how Rituxan treatment is progressing.
The relationship among all these players (and this is just the start of the full cast!) and Wegener’s is exceedingly complex. But to make it simple, B cells produce the antibodies to certain antigens that the immune system believes to be bad news. In autoimmune diseases, this “belief” turns out to be a mistake, at least in part. Of the many types of antibodies produced by the B cells, the kinds most involved with Wegener’s are called ANCA (Anti-Neutrophil Cytotoxic Antibodies. ANCA themselves come in at least two main forms: those that attack myeloperoxidase (MPO), and those that go after proteinase 3 (
PR-3). Under the microscope, A P-ANCA presentation is associated with anti-MPO; a C-ANCA presentation with anti-CP-3.
How the body becomes damaged from all this antibody activity is a long and fascinating story itself. But without opening that can of worms right now, the first item of business for any treatment plan is to clear out the rogue antibodies as much as possible, which is where prednisone (or prednisolone, the IV form) and plasma exchange come into the picture. The next goal is to prevent, or at least tame down, the production of new antibodies. This is what cytoxan and rituxan are supposed to accomplish. CTX bashes down the entire immune system; RTX targets just the B cells.
There are pluses and minuses to each approach. Neither is, in fact, ideal. Better yet would be to re-train the B cells to stop manufacturing ANCA. No one knows how to do this. Another line of therapy might be to intercept the ANCA before they can cause harm. There are, in fact, a couple of ideas on how to do this, though they are a long way from being part of the standard treatment program. We live in interesting times.
I hope this helps!
Al