Guillain-Barré syndrome is a common acute immune-mediated inflammatory disease of the PNS characterized by inflammatory infiltration and damage to myelin sheaths and axons. Experimental autoimmune neuritis (EAN) is an animal model for studying the pathogenesis and treatment of GBS. Many studies have confirmed that the pathogenesis and progression of GBS/EAN involve a variety of immune cell subsets and a complex network of cytokines. Th1, Th2, Th17, and Treg cells, the four common subsets of CD4+T cells, restrict or antagonize each other by releasing their effector cytokines. The net effects of Th cytokines determine the direction of immune responses and the consequence of GBS/EAN (Nyati et al., 2011; Zhang et al., 2013). A Th1 oriented response, which involves an increase in the production of Th1 cytokines, including IFN-γ, TNF-α, IL-1β, and IL-6, is associated with a GBS acute-phase reponse to the immune response after infection. During the recovery phase, the levels of IFN-γ were decreased and the IL-4 was increased, indicating that a Th2 response is related to recovery from the disease (Gigi et al., 2008). Th17 cells, which are independent of Th1 cells, have been reported to play an important role in the progression of the disease in humans and animal models. The proportion of Th17 cells in the peripheral blood and the levels of IL-17A in the plasma of patients with GBS were increased during the acute phase. Moreover, the levels of IL-17A are correlated with the GBS disability scale score (Li et al., 2012). Tregs, a subset of CD4+T cells which play a crucial role in the maintenance of immune tolerance and prevention of autoimmunity, are significantly reduced in GBS patients and EAN animals (Harness and McCombe, 2008). Macrophage-mediated segmental demyelination is the pathological hallmark of GBS/EAN. The pivotal role of macrophages in nerve damage during GBS/EAN involves the direct phagocytotic attack on myelin and the secretion of several pro-inflammatory cytokines, including IL-1, IL-6, IL-12, and TNF-α (Shen et al., 2018). Macrophages have been primarily divided into two distinct subsets: pro-inflammatory macrophages (M1) and anti-inflammatory macrophages (M2). M1 macrophages are involved in inflammatory impairments of the myelin sheath via the release of pro-inflammatory Th1 cytokines such as IL-12 during the early course of GBS (Labonte et al., 2014). In contrast, M2 macrophages are associated with recovery from the disease through the secretion of anti-inflammatory cytokines and the facilitation of Th2 immune responses in the later stage of GBS (Shen et al., 2018). These cells interact and promote each other, and even regulate the immune effect directly. The functions and interactions of these cells are mainly achieved through the secretion of cytokines. These cytokines are interconnected, complex, and pleiotropic, and constitute a complex immune network contributing to the pathogenesis of GBS/EAN (Zhang et al., 2013).