A Role for Interferon- β in Guillain-Barré Syndrome?

摘要: Guillain-Barre syndrome (GBS) is an acute inflammatory demyelinating neuropathy that associated with long-lasting morbidity and a substantial risk of mortality. The 2 reference treatments, plasma exchange intravenous immunoglobulins (IVIg), do not change the functional prognosis for most severely ill patients. pathogenesis GBS involves humoral cellular immune dysfunctions have only recently been characterised. Antibodies to nerve antigens may participate in complement activation, antibody-dependent macrophage cytotoxicity reversible conduction failure. reaction increases pro-inflammatory cytokines [such as tumour necrosis factor-alpha (TNFalpha)] matrix metalloproteinases (MMPs; e.g. MMP-9), decrease anti-inflammatory transforming growth factor-beta1 (TGFbeta1)]. All changes favour adhesion transmigration across endothelium cells, key phenomenon GBS. Recovery from characterised by normalisation these changes. Experimental allergic neuritis (EAN), experimental model GBS, has strikingly similar immunological characteristics. usual treatment options patients (plasma IVIg) mainly target component response. Interferon-beta (IFNbeta) immunomodulator inhibits antigen presentation TNFalpha production binding, modulates properties. IFNbeta T cell functions cytokines, such TGFbeta1. important effects on leukodiapedesis, caused modulating expression molecules MMP-9 proteinases. It used success EAN, some exacerbation chronic polyneuropathy, 1 patient pathophysiology understanding properties results studies support investigation trials