Neurotherapeutics

, Volume 4, Issue 4, pp 666–675

Modulating co-stimulation

Authors

    • Clinical Immunology Laboratory, Center for Neurologic DiseasesBrigham and Women’s Hospital and Harvard Medical School
  • Samia J. Khoury
    • Clinical Immunology Laboratory, Center for Neurologic DiseasesBrigham and Women’s Hospital and Harvard Medical School
Review Article

DOI: 10.1016/j.nurt.2007.07.006

Cite this article as:
Viglietta, V. & Khoury, S.J. Neurotherapeutics (2007) 4: 666. doi:10.1016/j.nurt.2007.07.006

Summary

The modulation of co-stimulatory pathways represents a novel therapeutic strategy to regulate autoimmune diseases. Auto-reactive CD4+ T cells play a critical role in initiating the immune response leading to inflammation and autoimmune diseases. Blocking co-stimulatory signals prevents T-cell activation, thus diminishing autoimmune responses and possibly preventing the progression of autoimmune disease. Blockade of several co-stimulatory pathways has been investigated in animal models and has led to clinical trials testing specific blocking agents in humans. In this review we will describe the role of co-stimulatory pathways, primarily the CD28-B7 pathway, in autoimmune diseases, and we will present in vivo and in vitro studies supporting the efficacy of co-stimulation blockade in animal models of autoimmune disease. Finally, we will discuss the clinical therapeutic efficacy of blocking monoclonal antibodies in preventing or reducing auto-antigen driven T-cell activation in humans with particular attention to the CD28/B7 pathway. Inhibiting co-stimulatory molecule interactions by using monoclonal antibodies seems to be an original approach to regulate autoimmune diseases in humans.

Key Words

T-cell activationCD28/B7 moleculesco-stimulation blockadeCT1A-4 IgEAE/MSmonoclonal antibody (mAb)
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Copyright information

© Springer New York 2007