Felix Heymann

Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice.

Role of T cells and dendritic cells in glomerular immunopathology.

CCR5 deficiency aggravates crescentic glomerulonephritis in mice.

The IL-23/Th17 axis contributes to renal injury in experimental glomerulonephritis.

Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury.

Monocytes and macrophages as cellular targets in liver fibrosis.

TAK1 suppresses a NEMO-dependent but NF-kappaB-independent pathway to liver cancer.

Kidney Dendritic Cells Become Pathogenic during Crescentic Glomerulonephritis with Proteinuria.

Role of IL-17 and Th17 cells in liver diseases.

Pharmacological inhibition of the chemokine CCL2 (MCP-1) diminishes liver macrophage infiltration and steatohepatitis in chronic hepatic injury.

Hepatic macrophage migration and differentiation critical for liver fibrosis is mediated by the chemokine receptor C-C motif chemokine receptor 8 in mice.

Peptide-functionalized gold nanorods increase liver injury in hepatitis.

Chemokine receptor CXCR6-dependent hepatic NK T Cell accumulation promotes inflammation and liver fibrosis.

YB-1 is an early and central mediator of bacterial and sterile inflammation in vivo.

Chemokine receptor CCR6-dependent accumulation of γδ T cells in injured liver restricts hepatic inflammation and fibrosis.

Pharmacological inhibition of the chemokine C-C motif chemokine ligand 2 (monocyte chemoattractant protein 1) accelerates liver fibrosis regression by suppressing Ly-6C(+) macrophage infiltration in mice.

Translation control of TAK1 mRNA by hnRNP K modulates LPS-induced macrophage activation.

CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN.