Why would chimeric antigen T-cell receptor therapy be appropriate for this condition? What are the inadequacies in the treatment landscape approaches like antibody therapy or bispecific therapy for this disease?

In pemphigus vulgaris, there is a history of using B-cell depleting agents.

I believe rituximab was approved in 2013 in the United States for pemphigus vulgaris.

Now, although patients do respond initially to rituximab depletion therapy, about, I'd say after two years, about 50% of patients relapse.

And there's been some interesting studies done where if you look at the clones that were present before and after rituximab therapy, you have the same autoreactive clones that are present.

that in pemphigus give rise to the short-lived antibody-secreting cells that secrete either DSG3 or DSG1 autoantibodies.

So there's a history of B cells being kind of the main target, the pathogenic bad actor, and with antibiotic therapies to deplete.

Is there anything about this being a skin disease that altered the way you think about how long you need persistence of the chimeric cells?