IL-23 Blockade for Crohn s disease: next generation of anti-cytokine therapy

Research output: Contribution to journalReview article

Abstract

Introduction: Adaptive immunity in intestinal inflammation may play a key role in the pathogenesis of Crohn’s disease. In particular, interleukin (IL)-23 may be a key mediator in chronic intestinal inflammation by inducing the differentiation of naïve CD4 + T cells into Th17, with the production of several pro-inflammatory cytokines. Furthermore, IL-23 induces interferon-γ (IFN- γ) production from activated T cells, a critical cytokine in innate and adaptive immunity against infections. Areas covered: We aim to review the available data from literature regarding the role of IL-23, with a more specific focus on the recent progresses in the therapeutic modulation of this cytokine. Expert commentary: Increased knowledge regarding the role of IL-23 has allowed for the development of effective therapeutic progresses by blocking the IL-23 mediated pathways. Primary or secondary loss of response to anti-TNF therapies in Crohn’s disease patients during the first year is widely described in literature: the development of new drugs, with alternative mechanisms of action, is thus a key point to consider for the optimal management of these subjects. Drugs blocking the IL-12/23 pathway showed a good efficacy and safety profile in immune-mediated diseases Further studies are necessary regarding the role of the single blockade of IL-23.

Original languageEnglish
Pages (from-to)457-467
Number of pages11
JournalExpert Review of Clinical Immunology
Volume13
Issue number5
DOIs
Publication statusPublished - May 4 2017

Keywords

  • anti-cytokine
  • biologics
  • Crohn’s disease
  • interleukin-23
  • ustekinumab

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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