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Number of items: 6.

Ribeiro, A; Wörnle, M; Anders, H J; Gröne, E F; Nitschko, H; Kurtschiev, P; Debiec, Hanna; Kretzler, M; Cohen, C D; Gröne, H J; Schlöndorff, D; Schmid, H (2012). Activation of innate immune defense mechanisms contributes to polyomavirus BK-associated nephropathy. Kidney International, 81(1):100-111.

Lichtnekert, J; Kulkarni, O P; Mulay, S R; Rupanagudi, K V; Ryu, M; Allam, R; Vielhauer, V; Muruve, D; Lindenmeyer, M T; Cohen, C D; Anders, H J (2011). Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1. PLoS ONE, 6(10):26778.

Jedlicka, J; Soleiman, A; Draganovici, D; Mandelbaum, J; Ziegler, U; Regele, H; Wüthrich, R P; Gross, O; Anders, H J; Segerer, S (2010). Interstitial inflammation in Alport syndrome. Human Pathology, 41(4):582-593.

Sayyed, S G; Hägele, H; Kulkarni, O P; Endlich, K; Segerer, S; Eulberg, D; Klussmann, S; Anders, H J (2009). Podocytes produce homeostatic chemokine stromal cell-derived factor-1/CXCL12, which contributes to glomerulosclerosis, podocyte loss and albuminuria in a mouse model of type 2 diabetes. Diabetologia, 52(11):2445-2454.

Lichtnekert, J; Vielhauer, V; Zecher, D; Kulkarni, O P; Clauss, S; Segerer, S; Hornung, V; Mayadas, T N; Beutler, B; Akira, S; Anders, H J (2009). Trif is not required for immune complex glomerulonephritis: dying cells activate mesangial cells via Tlr2/Myd88 rather than Tlr3/Trif. American Journal of Physiology: Renal Physiology, 296(4):F867-F874.

Vielhauer, V; Allam, R; Lindenmeyer, M T; Cohen, C D; Draganovici, D; Mandelbaum, J; Eltrich, N; Nelson, P J; Anders, H J; Pruenster, M; Rot, A; Schlöndorff, D; Segerer, S (2009). Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines. American Journal of Pathology:119-131.

This list was generated on Tue Oct 24 12:37:52 2017 CEST.