Transient immunosuppression: a bridge between infection and the atypical autoimmunity of Guillain–Barré syndrome?
Article first published online: 30 JUL 2010
© 2010 The Authors. Clinical and Experimental Immunology © 2010 British Society for Immunology
Clinical & Experimental Immunology
Volume 162, Issue 1, pages 32–40, October 2010
How to Cite
Steiner, I., Rosenberg, G. and Wirguin, I. (2010), Transient immunosuppression: a bridge between infection and the atypical autoimmunity of Guillain–Barré syndrome?. Clinical & Experimental Immunology, 162: 32–40. doi: 10.1111/j.1365-2249.2010.04223.x
- Issue published online: 9 SEP 2010
- Article first published online: 30 JUL 2010
- Accepted for publication 15 June 2010
- Guillain-Barré syndrome;
- immune mediated;
- infectious pathogens;
- transient immunosuppressed state
Guillain–Barré syndrome (GBS) is an acute, usually monophasic, disorder of the peripheral nervous system that is assumed to be of immune-mediated pathogenesis. However, several clinical features and experimental findings of GBS are uncharacteristic for an immune-mediated disorder and set this condition apart from other disorders with a putative immune-mediated pathogenesis. These features include, among others, the monophasic nature of GBS, the lack of response to immunosuppressive (unlike immunomodulatory) therapy, the absence of a typical association with immunogenetic background and the inability to establish a valid and relevant animal model. We suggest a comprehensive hypothesis for the pathogenesis of GBS that is based on the assumption that the condition is due to a transient (or occasionally chronic) immune deficiency, as in most cases GBS follows an infection with pathogens known to induce immunosuppression. Such infections may be followed by breakdown of immune tolerance and induction of an immune attack on peripheral nerves. Mounting of the immune-mediated assault might be triggered either by the same infective pathogen or by secondary infection. Clearance of the infection and resumption of a normal immune response and tolerance eventually terminate the immune-mediated damage to the peripheral nerves and enable recovery. This hypothesis assumes that the entire sequence of events that culminates in GBS is due to transient exogenous factors and excludes a significant role for inherent host susceptibility, which explains the monophasic nature of the disorder.