Targeting antibody-making cells may help hard-to-treat autoimmune disease

Early studies of drugs aimed at CD38 suggest benefits in lupus kidney disease and immune thrombocytopenia, but lasting effects and safety remain uncertain.

Editorial illustration — not from the study.

Long-lived plasma cells can continue making disease-causing antibodies even after conventional immune-suppressing treatments or therapies aimed at earlier stages of B-cell development. The review describes CD38 as a possible way to target these antibody-producing cells, drawing partly on experience using CD38-directed drugs in plasma-cell cancers.

The strongest evidence reviewed comes from lupus nephritis and immune thrombocytopenia, with additional early findings in autoimmune blood-cell disorders and AL amyloidosis, a disease linked to abnormal plasma cells. Reported benefits often occurred alongside rapid decreases in harmful autoantibodies, but questions remain about how long responses last and how best to use these treatments.

What the early studies found

The review finds that CD38-directed treatment has shown meaningful clinical and immune improvements in some severe, treatment-refractory autoimmune diseases. The most compelling evidence is in lupus nephritis and immune thrombocytopenia. Smaller proof-of-concept reports describe possible benefits in autoimmune cytopenias and plasma-cell-driven kidney disorders such as AL amyloidosis. These responses were often accompanied by rapid reductions in disease-causing autoantibodies.

Why antibody-making cells matter

If long-lived plasma cells are helping sustain disease, targeting them could address a source of harmful antibodies that conventional immune suppression and upstream B-cell treatments may not eliminate. This could provide another treatment approach for people whose autoimmune disease remains active or returns despite existing therapies. The review does not establish that CD38 treatment is effective or suitable for all autoimmune diseases.

Evidence and open questions

This is a review of the biological rationale and emerging clinical evidence, not a report of a single new clinical trial. The evidence is heterogeneous and comes largely from small cohorts, case series and early-phase trials. The abstract does not provide pooled effect sizes or a definitive comparison with standard treatment. Important uncertainties include how durable responses are, the best treatment strategy and long-term safety, particularly the risks of low antibody levels and infection.

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