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Moving targets: cell migration inhibitors as new anti-inflammatory therapies

Nature Immunology volume 9, pages 988–998 (2008)Cite this article

Abstract

The pharmaceutical industry has targeted various types of molecules to subdue inflammatory diseases. Drugs that disrupt cell migration appear particularly promising in clinical trials and in many animal models of inflammatory disease. Cell migration inhibitors not only interfere with migration of cells to a tissue, but also can affect other necessary processes such as mediator release and angiogenesis. However, the question is whether drugs that target adhesion molecules or chemoattractant receptors will prove superior to drugs that target other molecular types. This review proclaims the virtues of targeting cell migration–related molecules for development of new anti-inflammatory and anti-tumor based drugs. It is likely that cell migration inhibitors will transform the way in which many human inflammatory diseases and cancers are treated.

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Figure 1: Points where cell migration molecules operate during inflammatory responses.
Figure 2: An example of the use of a human-molecule knock-in mouse for drug discovery and validation.
Figure 3: Chemoattractants, cytokines and leukocyte types for different types of immune responses.

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Acknowledgements

I thank A. Rot, J.-C. Gutierrez Ramos and I. Mackay for helpful suggestions. Supported by the Australian National Health and Medical Research Council and the Cooperative Research Center for Asthma and Airways.

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  1. Garvan Institute for Medical Research, 384 Victoria Street, Darlinghurst, 2010, New South Wales, Australia

    Charles R Mackay

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Correspondence to Charles R Mackay.

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Competing interests

C.R.S. has equity in a small biotech company that developed and licensed to Novo Nordisk a drug that inhibits C5aR. He also has other commercially related interests around CXCR7 and CCR6.

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Mackay, C. Moving targets: cell migration inhibitors as new anti-inflammatory therapies. Nat Immunol 9, 988–998 (2008). https://doi.org/10.1038/ni.f.210

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