Daniel D. Pinschewer

This paper re-engineers a cytolytic viral vector to be non-cytolytic, enhancing CD8 T cell immunity through reinforced type I IFN signaling.

This study shows that chronic viral infection disrupts B cell affinity hierarchies by preferentially causing attrition of high-affinity B cells due to excessive antigen stimulation.

This study identifies IL-33 from oligodendrocytes as a key regulator of self-reactive CD8+ T cell differentiation in CNS autoimmunity and shows its potential as a therapeutic target.

This study introduces depletion-AAVs to permanently eliminate lymphocyte subsets in mice, showing B cells are critical for CD4 and CD8 T cell responses to chronic viral infection.