Selected Publications

Diehl C*, Soberón V*, Baygün S*, Chu Y*, …, Saur D, Steiger K, Rad R, Pasqualucci L, Weigert O, Schmidt-Supprian M. Hyperreactive B cells instruct their elimination by T cells to curb autoinflammation and lymphomagenesis. Immunity. 2025; 58(1):124-142.e15. doi: 10.1016/j.immuni.2024.11.023.

Bortoluzzi, S, … Rad, R., and Schmidt-Supprian, M. (2021). Brief homogeneous TCR signals instruct common iNKT progenitors whose effector diversification is characterized by subsequent cytokine signaling. Immunity 54, 2497-2513.e9. 10.1016/j.immuni.2021.09.003.

Kober-Hasslacher, M., …, Rudelius, M., and Schmidt-Supprian, M. (2020). c-Rel gain in B cells drives germinal center reactions and autoantibody production. Journal of Clinical Investigation 130, 3270–3286. 10.1172/jci124382. 

Vahl, J.C., … Klein, L., Korn, T., Sakaguchi, S., and Schmidt-Supprian, M. (2014). Continuous T Cell Receptor Signals Maintain a Functional Regulatory T Cell Pool. Immunity 41, 722–736. 10.1016/j.immuni.2014.10.012. 

Chu, Y., …, and Schmidt-Supprian, M. (2011). B cells lacking the tumor suppressor TNFAIP3/A20 display impaired differentiation and hyperactivation and cause inflammation and autoimmunity in aged mice. Blood 117, 2227–2236. 10.1182/blood-2010-09-306019.

Sasaki, Y., …, Rajewsky, K., and Schmidt-Supprian, M. (2008). NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells. PNAS 105, 10883–10888. 10.1073/pnas.0805186105. 

Sasaki, Y., … Reth, M., Rajewsky, K., and Schmidt-Supprian, M. (2006). Canonical NF-kappaB activity, dispensable for B cell development, replaces BAFF-receptor signals and promotes B cell proliferation upon activation. Immunity 24, 729–739.