Ralf Joachim Ludwig

This study shows that γδ T cell-derived IL-17A worsens experimental EBA, and IL-1β drives IL-17A production in these cells.

The paper identifies BTK as a therapeutic target in antibody-mediated autoimmune diseases by mapping FcγR signaling in neutrophils using kinase inhibitors and disease models.

The paper tests a CD19xCD3 bispecific T cell engager in a mouse model of pemphigoid disease and finds it induces remission in 45% of treated mice.

This study identifies ATP released from keratinocytes as a mediator of mechanical stress-induced NETosis in neutrophilic skin diseases, showing that ATP enhances C5a-induced NET formation and exacerbates inflammation.

This study shows that murine cytomegalovirus infection exacerbates inflammation in Pkp2 mutant mice but not in Ttn mutant mice, highlighting the interaction between genetic predisposition and environmental factors in cardiomyopathy.

The paper shows that in pemphigus, cell detachment, not autoantibody binding, causes long-term transcriptomic and proteomic changes associated with blister formation.