Neutralizing IL-23 and Its Targets May Improve Ankylosing Spondylitis

Imagine the implications. The investigators are describing how systemic cytokine expression could be initiated in one place in the body and have a tissue-specific pathology elsewhere in the body.

In an accompanying “News and Views” article, Rik J. Lories, MD, PhD, of KU Leuven in Belgium and Iain B. McInnes, PhD, at the University of Glasgow in the United Kingdom, wrote: “There have been a limited number of clinical trials targeting the IL-23–IL-17 axis in spondylarthritis, and such approaches have shown modest clinical benefits; these trials have focused mainly on strategies that neutralize IL-17. The data of Sherlock et al suggest that IL-23 mediates broader effects, operating beyond IL-17, and therefore the therapeutic utility of agents that block IL-23 or its receptor may be worthy of early exploration.”²

Spondylarthritis affects 2.4 million people in the United States and has a prevalence of 1% to 2% worldwide.

Dr. Pullen is a medical writer based in the Chicago area.

References

1. Sherlock JP, Joyce-Shaikh B, Turner SP, et al. IL-23 induces spondyloarthropathy by acting on ROR-γt+ CD3+CD4-CD8- entheseal resident T cells. Nat Med. 2012;18:1069-1076.

2. Lories RJ, McInnes IB. Primed for inflammation: Enthesis-resident T cells. Nat Med. 2012;18:1018-1019.