Complementary action of granulocyte macrophage colony-stimulating factor and interleukin-17A induces interleukin-23, receptor activator of nuclear factor-κB ligand, and matrix metalloproteinases and drives bone and cartilage pathology in experimental arthritis: rationale for combination therapy in rheumatoid arthritis

Lignende værker

• Blocking of Interleukin-17 during Reactivation of Experimental Arthritis Prevents Joint Inflammation and Bone Erosion by Decreasing RANKL and Interleukin-1
  af: Koenders, Marije I., et al.
  Udgivet: (2005)
• Interleukin-18 Promotes Joint Inflammation and Induces Interleukin-1-Driven Cartilage Destruction
  af: Joosten, Leo A.B., et al.
  Udgivet: (2004)
• Higher efficacy of anti-IL-6/IL-21 combination therapy compared to monotherapy in the induction phase of Th17-driven experimental arthritis
  af: Roeleveld, Debbie M., et al.
  Udgivet: (2017)
• Higher efficacy of anti-IL-6/IL-21 combination therapy compared to monotherapy in the induction phase of Th17-driven experimental arthritis.
  af: Debbie M Roeleveld, et al.
  Udgivet: (2017-01-01)
• Alteration of the intestinal microbiome characterizes preclinical inflammatory arthritis in mice and its modulation attenuates established arthritis
  af: Rogier, Rebecca, et al.
  Udgivet: (2017)