[Inhibition of the joint destruction in RA by TNF-blocking agents].
Tumor necrosis factor (TNF) -inhibitory biological response modifiers include neutralizing antibodies and receptor-immunoglobulin G (IgG) fusion proteins. These agents induce an amelioration of clinical signs and symptoms in most of the patients within a few weeks. Moreover, their inhibitory, or often repairing, effects on joint destruction are further excellent even in Japanese patients receiving a relatively lower dose of methotrexate (MTX) probably due to the direct inhibition of osteoclast activation through TNF.
Kameda
Hideto
H
Saitama Medical University, Department of Internal Medicine, Saitama Medical Center, Division of Rheumatology Clinical Imunology.
D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology*; D018450:Disease Progression; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069285:Infliximab; D007596:Joints / Q000473:pathology*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000502:physiology*
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept