Abstract
The two possibilities to explain the pathogenic basis of stiff-person syndrome (SPS) are intrathecal sensitization of GAD65-reactive CD4+T cells and synthesis of GAD65-specific autoantibodies within the CNS [Rakocevic et al., Arch. Neurol. 61: 902-904, 2004]; and peripheral antigen sensitization followed by CNS antigen recognition by autoantibodies that cross the blood-brain barrier. Antigen-specific CD4+ T cells are essential for the generation of high-affinity autoantibodies [Lanzavecchia, Nature 314: 537-539, 1985], but there is no evidence of cellular infiltration in the CNS of SPS patients [Warich-Kirches et al., Clin. Neuropathol. 16: 214-219, 1997; Ishizawa et al., Acta Neuropathol.(Berl) 97: 63-70, 1999]. This review discusses the possible role of autoantibodies and autoreactive T cells specific to neuronal antigens in SPS pathogenesis.
Original language | English (US) |
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Pages (from-to) | 79-92 |
Number of pages | 14 |
Journal | International Reviews of Immunology |
Volume | 27 |
Issue number | 1-2 |
DOIs | |
State | Published - Jan 2008 |
Externally published | Yes |
Keywords
- Autoimmunity
- Gamma aminobutyric acid (GABA)
- Glutamic acid decarboxylase autoantibodies
- Stiff-person syndrome
- T cells
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology