Can IFN-γ be a therapeutic target in Guillain-Barré syndrome?

INTRODUCTION

Guillain-Barré syndrome (GBS) is an immune-mediated acute inflammatory disorder of the PNS in humans characterized by inflammatory infiltration and damage to myelin and axon. Experimental autoimmune neuritis (EAN) is a useful animal model for studying the pathogenesis and treatment of GBS. Immunocompetent cells together with cytokines produced by various cells contribute to the inflammatory process of GBS and EAN by acting as mediators or effectors.

AREAS COVERED: Both GBS and EAN have long been attributed to T helper (Th) 1 cell-mediated autoimmune disorders. IFN-γ acts as a central mediator of Th1-mediated autoimmune disorders by deflecting the immune response toward a Th1 phenotype by inducing the differentiation of T cells to a Th1 phenotype and inhibiting the development of Th2 cells in autoimmune disorders such as GBS. In this review, we present an overview of current knowledge on the inflammatory and immunoregulatory role of IFN-γ in GBS and EAN, which is important for evaluating whether IFN-γ can become a potential therapeutic target in GBS.

EXPERT OPINION: Analysis of immunopathogenesis of GBS and EAN revealed the significance of IFN-γ in both diseases, even though the complex mechanism of the delicate modulation of the cytokine is still under debate. More work needs to be done to rule out its potential in immunoregulatory function and pave the way for new therapeutic strategies for GBS.