Oh please keep the “verbiage” so this keeps an NC-17 rating. I can tell my dad that I’m still doing good stuff with my career.

Similar to how the medical world realized how over-reliant they’ve been on elective procedures for generating revenue, academic institutions similarly got lazy. How they innovate around this will be interesting, and way above my pay grade.

I don’t buy that federal grants are better because they are longer and have higher direct cost caps: these grants still do not cover the true costs for the research funded anyway.

Hmmm.

Part of this is the fault of academic institutions IMO: the financial reliance on governmental indirect costs led to the strong link to get federal grants for faculty promotion. No matter how many grants you get from private foundations, lack of governmental funding is a strike against you.

Our hospital system (Barnes-Jewish) uses the Mayo Clinic Labs “CRY-S” (www.mayocliniclabs.com/test-catalog...) test, which is cryocrit-based with a reflex immunofixation. What is this Ig quant test, never heard of it!

I feel that the antigen will always be there, and coupled with any memory responses, there could be persistent activation of these B cells.

So RTX does not deplete B cells from lymph nodes & likely inflamed organs.

Curious in the non-responders what the C3 nephritic factor levels are. If high, they are coming from long-lived plasma cells (I’d hypothesize). If they drop, then it argues that tissue B cells are contributing to pathology.

Good question: depends if it is coming from plasmablast or plasma cells. Most SLE autoAbs come from extrafollicular activated B cells that differentiate into “pre-plasma cells,” which are plasmablast precursors. They are indirectly depleted with RTX.

pubmed.ncbi.nlm.nih.gov/30314758/

Sounds like we need to look, and yes, @anujajava.bsky.social has asked me before. We have ~400 patients with classified lupus we could query.