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T Follicular Helper-Like Cells Are Involved in the Pathogenesis of Experimental Autoimmune Encephalomyelitis
T Follicular Helper-Like Cells Are Involved in the Pathogenesis of Experimental Autoimmune Encephalomyelitis
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T Follicular Helper-Like Cells Are Involved in the Pathogenesis of Experimental Autoimmune Encephalomyelitis
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T Follicular Helper-Like Cells Are Involved in the Pathogenesis of Experimental Autoimmune Encephalomyelitis
T Follicular Helper-Like Cells Are Involved in the Pathogenesis of Experimental Autoimmune Encephalomyelitis
Journal Article

T Follicular Helper-Like Cells Are Involved in the Pathogenesis of Experimental Autoimmune Encephalomyelitis

2018
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Overview
Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) have been proved to be T cell-mediated autoimmune diseases. Recent researches indicate that humoral immunity is also involved in the pathogenesis of these disorders. T follicular helper (Tfh) cells are critical for B cell differentiation and antibody production. However, the role of Tfh cells in MS and EAE remains unclear. Here, we found elevated frequencies of CD4 CXCR5 PD-1 Tfh-like cells in both MS patients and EAE. In EAE mice, Tfh-like cells, together with B cells, were found in the ectopic lymphoid structures in spinal cords. Moreover, Tfh-like cells promoted the antibody production IL-21/IL-21R and CD40 ligand/CD40 interaction and the synergy effect of STAT3 and non-canonical NF-κB signaling pathway inside B cells. Moreover, adoptive transfer of Tfh-like cells could increase the severity and delay the remission of EAE. In conclusion, our data indicate that Tfh-like cells contribute to the pathogenesis of EAE.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject

Adoptive transfer

/ Adult

/ Animals

/ Antibodies

/ Autoantibodies - immunology

/ Autoimmune diseases

/ Autoimmunity

/ B-Lymphocytes - immunology

/ B-Lymphocytes - metabolism

/ Brain - immunology

/ Brain - metabolism

/ Brain - pathology

/ CD4 antigen

/ CD4-Positive T-Lymphocytes - immunology

/ CD4-Positive T-Lymphocytes - metabolism

/ CD40 antigen

/ CD40 ligand

/ Cell differentiation

/ Cells

/ CXCR5 protein

/ Cytokines - metabolism

/ Disease Models, Animal

/ Encephalomyelitis

/ Encephalomyelitis, Autoimmune, Experimental - etiology

/ Encephalomyelitis, Autoimmune, Experimental - metabolism

/ Encephalomyelitis, Autoimmune, Experimental - pathology

/ Experimental allergic encephalomyelitis

/ experimental autoimmune encephalomyelitis

/ Female

/ Flow cytometry

/ Germinal Center - immunology

/ Germinal Center - metabolism

/ Germinal Center - pathology

/ Humans

/ Humoral immunity

/ Immunology

/ interlukin-21

/ Laboratories

/ Lymphocyte Activation

/ Lymphocyte Count

/ Lymphocytes B

/ Lymphocytes T

/ Male

/ Mice

/ Middle Aged

/ Multiple sclerosis

/ Multiple Sclerosis, Relapsing-Remitting

/ Myelin-Oligodendrocyte Glycoprotein - adverse effects

/ NF-κB protein

/ Pathogenesis

/ PD-1 protein

/ Peptide Fragments - adverse effects

/ Peptides

/ Remission

/ Remission (Medicine)

/ Signal transduction

/ Spinal Cord - immunology

/ Spinal Cord - metabolism

/ Spinal Cord - pathology

/ Stat3 protein

/ T follicular helper cells

/ T-Lymphocytes, Helper-Inducer - immunology

/ T-Lymphocytes, Helper-Inducer - metabolism

/ Young Adult