Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments

Abstract

The Guillain-Barré syndrome (GBS) is considered a T helper 1 (Th1) cells-mediated acute inflammatory peripheral neuropathy. However, some changes in GBS could not be explained completely by Th1 cells pathogenic role. Recently, Th17 cells have been identified and can mediate tissue inflammation and autoimmune response. Therefore, a study on the role of Th17 and Th22 cells and their cytokines in GBS is necessary for exploring the pathogenesis of GBS. Here, we detected the frequency of Th1, Th17, and Th22 cells by using 4-color flow cytometry and we detected the plasma levels of IL-17 and IL-22 by ELISA in GBS patients, relapsing-remitting multiple sclerosis patients at the acute phase of relapse, viral encephalitis or meningitis patients and healthy controls. Our data showed that the frequency of circulating Th1, Th17, and Th22 cells was significantly increased in GBS patients. The plasma levels of IL-17 and IL-22 in GBS and relapsing-remitting multiple sclerosis at the acute phase of relapse were also markedly elevated. Enhanced circulating Th22 cells were correlated with GBS severity. Intravenous immunoglobulin therapy downregulated Th17, and Th22 cells and the plasma levels of IL-17 and IL-22 in GBS patients. Th17 and Th22 cells may be involved in the pathogenesis of GBS, and intravenous immunoglobulin mediates therapeutic effects by downregulating these cells and their cytokines.

Guillain-Barré syndrome: causes, immunopathogenic mechanisms and treatment

“…jejuni induces the unbalance of Th1/Th2/Th17/Treg and cytokines that is crucial for the development of GBS [14]. In addition, Th17 also plays a pathogenic role, and elevated circulating Th22 cells are correlated with severity of disease, but not with GBS subphenotypes [48]. In addition, Th17 also plays a pathogenic role, and elevated circulating Th22 cells are correlated with severity of disease, but not with GBS subphenotypes [48].…”

“…Up regulation of Th1 cytokines in the early disease course may be associated with immune-mediated disease progression due to neuronal inflammation, but up regulation of Th2 immune response during the later phase aids recovery from the disease [47]. Th17 and Th22 cells of GBS patients at acute phase could express an appropriate cytokine profile, like IL-17, IL-22, and others (IL-6 and TNF-), which can enhance the inflammatory and autoimmune response and conduce to the development of GBS [48]. Th17 and Th22 cells of GBS patients at acute phase could express an appropriate cytokine profile, like IL-17, IL-22, and others (IL-6 and TNF-), which can enhance the inflammatory and autoimmune response and conduce to the development of GBS [48].…”

T cell epitope redundancy: cross-conservation of the TCR face between pathogens and self and its implications for vaccines and autoimmunity

“…Although no studies have identified specific T cell epitopes involved, it is clear that their formation is T cell-dependent. Several populations of T-helper cells have been identified in cases of C. Jejuni-induced GBS [78], and immunoglobulin class-switching has been observed in transgenic mice that lack complex ganglioside when immunized with C. Jejuni LPS [79]. Evaluation of potential cross-reactivity between GBS-associated antigens in pathogens and self is both feasible and actionable using JanusMatrix.…”

Immune camouflage: Relevance to vaccines and human immunology

“…36 Applications of JanusMatrix may be relevant, therefore, in the context of autoimmune diseases following vaccination, such as Guillain-Barre syndrome or Narcolepsy. [37][38][39] Finally, pathogen subterfuge may teach us something about our own immune system. What is the role of human peptide epitopes that are themselves cross-reactive with other human sequences?…”