research interests
research programs
medical thesis program
Ph.D. program
Research interests

We are interested in the immune system`s contribution to the initiation and progression of kidney disease. As part of that we focus and distinct aspects of innate and adaptive immunity:

Regarding innate immunity, we assume that

  • The immune system is a guardian of kidney homeostasis
  • The immune system modulates all phases of kidney injury to regain homeostasis
    • The immune system promotes kidney inflammation upon infection to support host defens
    • The immune system promotes sterile kidney inflammation in a similar manner as an atavism of evolutional selection for host defense
    • Inflammation and renal cell death trigger each other in an auto-amplification-loop, i.e. necroinflammation (Linkermann et al. Nat Rev Immunol 2014). DAMP-mediated TLR/inflammasome activation and regulated cell necrosis are essential in this process
    • The immune system promotes kidney regeneration upon resolution of inflammation, i.e. re-epithelialization of glomeruli and tubules whenever sufficient intrinsic regenerative elements survived the injury, renal fibrosis to mechanically stabilize those nephrons that survived the injury phase. This implies that the immune system promotes nephron loss and subsequent diffuse renal fibrosis in chronic injuries with persistent inflammation.
  • Blocking renal inflammation and/or cell death in the injury phase saves nephrons from injury, enforces intrinsic kidney regeneration, and prevents renal fibrosis in AKI and CKD.

Regarding adaptive immunity, we assume that

  • The genetic heterogeneity of the population is also present in the immune system, which explains many if not most of the immune-mediated glomerular disorders (Kurts et al. Nat Rev Immunol 2013).
  • The common pathway of all forms of glomerulonephritis is (auto) antigen-presentation via MHC-II in antigen-presenting cells (DCs and B cells).
  • This largely explains the efficacy of Rituximab in autoimmune diseases rather than the assumed effects on B1 cells or autoantibody production.
  • MCH-II is a very promising therapeutic target for all sorts of auto- or alloimmune kidney disorders.
  • Another topic of our interest is the immunoregulatory effect of CD362+ mesenchymal stem (stroma) cells (EU Networks REDDSTAR and NEPHSTROM).


Dr. H.-J- Anders, Dr. V. Vielhauer, anders & vielhauer, research laboratory, research interests, research programs, medical thesis program, Ph. D. program, publications, protocols, Leukocyte activation, Renal cell activation, Leukocyte migration, Target identification program, Target validation program, Drug validation program in disease models, Clinical Science