Inflammation: Treatment Progress and Limitations

Clin Pharmacol Ther. 2017 Oct;102(4):564-567. doi: 10.1002/cpt.792.

Abstract

There is an increasing understanding on the etiology of chronic immune-mediated inflammatory diseases such as inflammatory bowel disease (IBD), psoriasis, or rheumatoid arthritis. Large consortia contributed to the elucidation of the genetics, for instance, of IBD identifying a number of genes involved in innate mucosal defense and immune tolerance (most prominent, e.g., NOD2) and other related processes. For a number of such diseases, common genetic susceptibility loci were identified, suggesting overlapping immune response pathways, although there is no causality of single genetic traits.2 In particular, the elucidation of main triggers of inflammation like tumor necrosis factor alpha (TNFα), integrins, specific cytokines like interleukin (IL)-6 or IL-23 launched the successful development of new pharmacological approaches, leading to a tremendous improvement of therapeutic outcomes.

Publication types

  • Editorial

MeSH terms

  • Arthritis, Rheumatoid / drug therapy
  • Arthritis, Rheumatoid / genetics
  • Arthritis, Rheumatoid / pathology
  • Cytokines / immunology
  • Drug Design*
  • Genetic Predisposition to Disease*
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / genetics
  • Inflammation / pathology
  • Inflammatory Bowel Diseases / drug therapy
  • Inflammatory Bowel Diseases / genetics
  • Inflammatory Bowel Diseases / pathology
  • Psoriasis / drug therapy
  • Psoriasis / genetics
  • Psoriasis / pathology

Substances

  • Cytokines