@BeckySueToo @RheumJC Let me explain...
@BeckySueToo @RheumJC What is wrong here is using total B cells. There are sunsets of CD19. Broadly speaking: naive (have not received Ag stimulation, not activated and no T cell help); memory (antigen experiences, been in a terminal centre) and plasmablast (trying to become a plasma cell)...
@BeckySueToo @RheumJC In healthy people B cells are about 2/3 naive, 1/3 memory, 1-2% plasmablast. But in autoimmune diseases this changes. In SLE the hallmark is expansion of the plasmablasts, up to 5 or even 10%. Makes sense, right? #rheumjc
@BeckySueToo @RheumJC When we treat an SLE patient with rituximab, if the early returning be cells are mostly plasmablasts this is a BAD sign. This is the signature of active SLE. They are heading for relapse and need more rituximab. We validated this in 150 patients. #rheumjc
@BeckySueToo @RheumJC Now then, what about AAV? I’ll be a few minutes finding a pic from our paper... #rheumjc
@BeckySueToo @RheumJC What AAV patients have (before rituximab) is naive lymphopenia. Worse activity (eg high CRP) = more lymphopenic. 
@BeckySueToo @RheumJC Here fig A is the situation before rituximab in AAV. HC = healthy control. B is repeat measurements during a cycle of rituximab in three diseases.
@BeckySueToo @RheumJC Do you notice the way that the naive lymphopaenia recurs in early repopulation by 6 months in the AAV group? Is that a good sign for these patients? I don’t think so. Naive lyphopenia is the signature of active AAV. #rheumjc
@BeckySueToo @RheumJC So. Is return of CD19+ cells (which are mostly naive) going to be a good sign or a bad sign in this particular disease? #rheumjc
@BeckySueToo @RheumJC This is why they saw relapses with low B cells.
