What have been the reactions of rheumatologists and other clinicians to the Nature Medicine paper results?

Is there a belief that this therapy could be applied to a large majority of SLE patients or only the most severely affected? Are there different SLE phenotypes in which you think the treatment might not work?

 It would be helpful if for the various CD-19 CAR programs targeting SLE you could differentiate between the different constructs, including the one you studied in the Erlangen study, what Kyverna is studying for Lupus Nephritis, and also Cabaletta Bio’s construct. What are the structural differences and how could they impact development timelines and results? For example, does Cabaletta Bio’s CD-3 Zeta signaling domain component make a difference or not? How important is the fully human binder used? Are there sources of differentiation that could manifest in manufacturing and cell delivery processes?

Are you aware of efforts by the big pharma companies to venture into CAR-T for autoimmune diseases with similar efforts?

What are some of the key hurdles you expect to show proof of concept long term, both in registrational settings and with the Erlangen study? For example, how long do you think you need to show sustained remissions before you can be confident patients won’t relapse?

At an ACR presentation last fall there was a slide in your presentation that mentions 10 patients treated successfully. What can you tell us about the 5 other patients not included in the Nature Medicine paper?

 A study was recently published in Science Immunology by folks at the Washington School of Medicine (Jaeu Yi lead author) where the CAR attaches to Multiple Sclerosis-related helper T cells in mice. They ran into some binding issues but through some iteration they devised CAR Ts that can target t-cells affecting MS induction and separately other t-cells that improve MS clinical symptoms. It’s unclear if this would be just therapeutic vs curative. I wondered if you had any thoughts on this approach or tackling an indication like Multiple Sclerosis in general with CAR T.  

What are the differences with other indications such as SLE, Rheumatoid Arthritis, Myositis and Systemic Sclerosis, and how could they be overcome? Are there other autoimmune indications where you think similar CD-19 constructs could be applied?

When I spoke with Gerhard Kronke he mentioned your group is working on some molecular studies to see how B-cells and T-cell phenotypes change over time in SLE patients. What fundamental questions are you trying to answer with that work?

 I’ve heard you tried a patient with a reduced conditioning regimen. Do you believe these treatments will eventually be possible without a conditioning regimen?

Do you plan to release more updates on the Erlangen study in 2023?

Cabaletta recently licensed an RQR8 safety switch technology from Autolus therapeutics. What is your view on how this might be used in future iterations of cell therapy, if necessary?

What future studies are you interested in pursuing in this space?