Aberrant Dendritic Cell Subsets in Patients with Myasthenia Gravis and Related Clinical Features.

Introduction: Dendritic cells (DCs) play critical roles in the pathogenesis of myasthenia gravis (MG), and a series of DC-based experimental strategies for MG have recently been developed. However, the definite roles of different DC subsets in the mechanism of MG have scarcely been covered by previous studies. The present study aimed to investigate the levels of three main DC subsets, plasmacytoid DCs (pDCs) (CD303 positive) and two distinct subsets of conventional DCs (cDCs), namely CD1c+ cDCs and CD141+ cDCs, in MG patients and analyze related clinical features.

Asymmetric limb weakness in Guillain-Barré syndrome: Three case reports.

Background: Guillain-Barré syndrome (GBS) is an autoimmune-mediated peripheral neuropathy characterized by symmetric weakness. Asymmetric weakness in GBS is uncommon and may be easily confused with other differential diagnoses. We herein present three cases of asymmetric GBS and review the literature on this atypical subtype of GBS in order to describe the characteristics of asymmetric GBS and to provide experience for clinicians.

[Severe encephalitis caused by infection of Rickettsia felis: a case report].

Rickettsia felis is a Gram-negative prokaryotic organism that is obligatorically parasitic in cells. Cat fleas are the main vector of Rickettsia felis. Clinical symptoms of human infection with Rickettsia felis include fever, fatigue, headache, macular papules, and eschar.

Guillain-Barré syndrome in Eastern China: A study of 595 patients.

Background And Purpose: This study aimed to investigate geographical differences in the clinical features of Guillain-Barré syndrome (GBS) between patients from our region in Eastern China and patients from other areas.

Methods: A total of 595 patients fulfilling the diagnostic criteria ​for GBS or its variants were included from two large hospitals located in Eastern China. Data collection included demographics, antecedent events, clinical presentation and signs, electrophysiological subtypes, treatment, complications during hospitalization, clinical severity at nadir, and outcome at 12 months, and these data were compared to data from a study conducted in Southern China and the Europe/Americas section of the International GBS Outcome Study.

Co-occurrence of Moyamoya syndrome and Kartagener syndrome caused by the mutation of DNAH5 and DNAH11: a case report.

Background: Kartagener syndrome is an autosomal recessive inherited disorder of primary ciliary dyskinesia. Moyamoya syndrome refers to a moyamoya angiopathy associated with other neurological and/or extra-neurological symptoms, or due to a well identified acquired or inherited cause. We herein reported a case of a 48-year-old woman who was favored the diagnosis of Kartagener syndrome and moyamoya syndrome.

Antecedent infections in Guillain-Barré syndrome: a single-center, prospective study.

Objective: To investigate the spectrum of antecedent infections in Chinese patients with Guillain-Barré syndrome (GBS) and analyze the infections-related clinical phenotypes locally.

Methods: A prospective case-control study of 150 patients diagnosed with GBS and age- and sex-matched neurological and healthy controls was performed to investigate recent infections of 14 pathogens serologically and collect the clinical data during a follow-up of 12 months.

Results: In total, 53% of patients with GBS had a positive serology for recent infection, including Campylobacter jejuni (27%), influenza A (17%) and B (16%), hepatitis A virus (5%), dengue virus (3%), cytomegalovirus (3%), Epstein-Barr virus (3%), Mycoplasma pneumoniae (2%), herpes simplex virus (2%), varicella-zoster virus (1%), and rubella virus (1%).

Intravenous immunoglobulin promotes the proliferation of CD4CD25 Foxp3 regulatory T cells and the cytokines secretion in patients with Guillain-Barré syndrome in vitro.

Intravenous immunoglobulin (IVIg) serves as the first line therapy in Guillain-Barré syndrome (GBS), however, its action mechanism remains unknown. We hereby stimulated peripheral blood mononuclear cells (PBMCs) from patients with GBS and healthy controls using IVIg and an IgG-derived natural Treg epitopes, namely Tregitopes. Our results showed that IVIg significantly promoted both the expansion of CD4CD25Foxp3 regulatory T cells (Tregs) and secretion of IL-10 and TGF-β1 while Tregitopes promoted secretion of IL-10 and TGF-β1 only.

Memory B cells in Guillain-Barré syndrome.

IgG autoantibodies against gangliosides show the highest titers at the disease onset of axonal Guillain-Barré syndrome (GBS), in which there are no IgM anti-ganglioside antibodies. We hypothesized that memory B cells take part in the development of producing IgG autoantibodies. In this study, we analyzed the memory B cells in patients with GBS using flow cytometry.

Vinpocetine Inhibited the CpG Oligodeoxynucleotide-induced Immune Response in Plasmacytoid Dendritic Cells.

Plasmacytoid dendritic cells (pDCs) exert dual roles in immune responses through inducing inflammation and maintaining immune tolerance. A switch of pDC phenotype from pro-inflammation to tolerance has therapeutic promise in the treatment of autoimmune diseases. Vinpocetine, a vasoactive vinca alkaloid extracted from the periwinkle plant, has recently emerged as an immunomodulatory agent.

Increased plasmacytoid dendritic cells in Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is a post-infectious autoimmune disease. Dendritic cells (DCs) can recognize the pathogen and modulate the host immune response. Exploring the role of DCs in GBS will help our understanding of the disease development.

Suppressive oligodeoxynucleotides induced tolerogenic plasmacytoid dendritic cells and ameliorated the experimental autoimmune neuritis.

Toll-like receptor (TLR) 9, recognizing different ligands, confers distinct features of plasmacytoid dendritic cells (pDCs). Our previous study demonstrated a role for TLR9 in the mechanism of experimental autoimmune neuritis (EAN). In this study, we explored whether suppressive oligodeoxynucleotides (sODN) could induce tolerogenic pDCs via TLR9 and thus promote the recovery of EAN.

A novel and functional variant within the ATG5 gene promoter in sporadic Parkinson's disease.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Majority of PD are sporadic, for which genetic causes remain largely unknown. Alpha-synuclein, the main component of Lewy bodies, plays a central role in the PD pathogenesis.

Genetic analysis of the ATG7 gene promoter in sporadic Parkinson's disease.

Parkinson's disease (PD) is the second most common neurodegenerative disease. The majority of PD cases are sporadic, for which genetic causes and underlying molecular mechanisms remain largely unclear. Autophagy, a highly conserved cellular process that governs the breakdown of long-lived proteins and organelles, has been involved in the degradation of α-synuclein (α-Syn), the main component of Lewy bodies.

Silencing of miR155 promotes the production of inflammatory mediators in Guillain-Barré syndrome in vitro.

MicroRNA-155 (miR155) has been demonstrated as a central regulator of immune responses induced by inflammatory mediators. Previous studies suggest that miR155 may play adverse effects in various diseases. We hereby explored the roles of miR155 in the pathogenesis of Guillain-Barré syndrome (GBS).

Genetic analysis of lysosomal alpha-galactosidase A gene in sporadic Parkinson's disease.

Parkinson's disease (PD) is a progressive neurodegenerative disease. Majority of PD cases are sporadic, resulting from interaction of genetic and environmental factors. Accumulating evidence indicates that autophagy, which delivers alpha-synuclein to lysosomes for degradation, is involved in the PD pathogenesis.

Decreased expression of lysosomal alpha-galactosiase A gene in sporadic Parkinson's disease.

Parkinson's disease (PD) is a progressive neurodegenerative disease. To date, the causal genes and variants associated with sporadic PD are largely unknown. Accumulating evidence demonstrates that autophagy delivers alpha-syncuclein proteins to lysosome for degradation and dysfunctional autophagy is involved in the PD pathogenesis.

Altered expression of autophagic genes in the peripheral leukocytes of patients with sporadic Parkinson's disease.

Parkinson's disease (PD) is a progressive neurodegenerative disease caused by interaction of genetic and environmental factors. To date, genetic genes and variants causing PD remain largely unknown. Autophagy is a conserved cellular process including three subtypes, macroautophagy (hereafter referred to as autophagy), microautophagy and chaperone-mediated autophagy (CMA).

Decreased activities of lysosomal acid alpha-D-galactosidase A in the leukocytes of sporadic Parkinson's disease.

Parkinson's disease (PD) is a progressive neurodegenerative disease that affects aged people. Although a number of genes have been linked to familial PD, the genetic causes of sporadic PD that accounts for 90% of all PD cases remain unclear. Accumulating evidence has demonstrated that alpha-synuclein aggregation is essential to the pathogenesis of PD.