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Inflammation: Treatment Progress and Limitations
Author(s) -
Cascorbi Ingolf
Publication year - 2017
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt.792
Subject(s) - rheumatoid arthritis , immunology , nod2 , inflammation , immune system , psoriasis , inflammatory bowel disease , tumor necrosis factor alpha , disease , etiology , medicine , innate immune system , biology , bioinformatics , pathology , psychiatry
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.[1][Khor, B., 2011] 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.