Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms

Mu, Lili; Zhang, Yao; Sun, Bo; Wang, Jinghua; Xie, Xin; Li, Na; Zhang, Jia; Kong, Qingfei; Liu, Yumei; Han, Zhijuan; Wang, Guangyou; Zheng, Fuli; Yu, Bo; Li, Guozhong; Li, Hulun

doi:10.1016/j.clim.2011.04.013

Cited by 27 publications

(19 citation statements)

References 35 publications

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“…The percentage of IL-9-producing CD4 + T cells increases during EAMG progression EAMG presents in two clinical phases: the early phase, at around 8-14 days post-immunization; 31,32 and the chronic phase, beginning approximately 40 days after primary immunization. To determine the percentage of Th9 cells present during the different stages of EAMG, we isolated MNCs from the LNs of rats in the CFA and EAMG groups during the early and chronic phases.…”

Section: Resultsmentioning

confidence: 99%

Neutralization of interleukin‐9 ameliorates symptoms of experimental autoimmune myasthenia gravis in rats by decreasing effector T cells and altering humoral responses

et al. 2014

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SummaryInterleukin-9 (IL-9) was initially thought to be a type 2 T helper (Th2) -associated cytokine involved in the regulation of autoimmune responses by affecting multiple cell types. However, it was recently shown that IL-9-producing CD4 + T cells represent a discrete subset of Th cells, designated Th9 cells. Although Th9 cells have been shown to be important in many diseases, their roles in myasthenia gravis (MG) are unclear. The aim of this study was to determine whether IL-9 and Th9 cells promote the progression of experimental autoimmune myasthenia gravis (EAMG).The results showed that the percentage of Th9 cells changed during the progression of EAMG, accompanied by an up-regulation of IL-9. Blocking IL-9 activity with antibodies against IL-9 inhibited EAMG-associated pathology in rats and reduced serum anti-acetylcholine receptor IgG levels. Neutralization of IL-9 altered the Th subset distribution in EAMG, reducing the number of Th1 cells and increasing the number of regulatory T cells. Administration of an anti-IL-9 antibody may represent an effective therapeutic strategy for MG-associated pathologies or other T-cell-or B-cell-mediated autoimmune diseases.

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Section: Resultsmentioning

confidence: 99%

Neutralization of interleukin‐9 ameliorates symptoms of experimental autoimmune myasthenia gravis in rats by decreasing effector T cells and altering humoral responses

et al. 2014

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“…S100B also stimulates RAGE-mediated proliferation of T cells directed to the acetylcholine receptor and upregulation of cyclo-oxygenase 2 expression in splenocytes, implicating the S100B/RAGE axis in the pathogenesis of myasthenia gravis [334]. S100B is expressed in, and secreted by CD8 + T lymphocytes and NK cells [153], thus potentially participating in the innate immune response, as outlined above, and in the adaptive immune response via RAGE engagement.…”

Section: Extracellular Functions Of S100 Proteinsmentioning

confidence: 99%

“…S100B is expressed in, and secreted by CD8 + T lymphocytes and NK cells [153], thus potentially participating in the innate immune response, as outlined above, and in the adaptive immune response via RAGE engagement. The disparate effects of S100B [12,334], i.e. resolution and exacerbation of inflammation by the S100B/RAGE axis, respectively, are likely to depend on different types of responding cells coming into play in two conditions and differences in S100B doses and levels of RAGE expression.…”

Section: Extracellular Functions Of S100 Proteinsmentioning

confidence: 99%

Functions of S100 Proteins

Donato¹,

Cannon²,

Sorci³

et al. 2013

Current Molecular Medicine

1,092

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The S100 protein family consists of 24 members functionally distributed into three main subgroups: those that only exert intracellular regulatory effects, those with intracellular and extracellular functions and those which mainly exert extracellular regulatory effects. S100 proteins are only expressed in vertebrates and show cell-specific expression patterns. In some instances, a particular S100 protein can be induced in pathological circumstances in a cell type that does not express it in normal physiological conditions. Within cells, S100 proteins are involved in aspects of regulation of proliferation, differentiation, apoptosis, Ca2+ homeostasis, energy metabolism, inflammation and migration/invasion through interactions with a variety of target proteins including enzymes, cytoskeletal subunits, receptors, transcription factors and nucleic acids. Some S100 proteins are secreted or released and regulate cell functions in an autocrine and paracrine manner via activation of surface receptors (e.g. the receptor for advanced glycation end-products and toll-like receptor 4), G-protein-coupled receptors, scavenger receptors, or heparan sulfate proteoglycans and N-glycans. Extracellular S100A4 and S100B also interact with epidermal growth factor and basic fibroblast growth factor, respectively, thereby enhancing the activity of the corresponding receptors. Thus, extracellular S100 proteins exert regulatory activities on monocytes/macrophages/microglia, neutrophils, lymphocytes, mast cells, articular chondrocytes, endothelial and vascular smooth muscle cells, neurons, astrocytes, Schwann cells, epithelial cells, myoblasts and cardiomyocytes, thereby participating in innate and adaptive immune responses, cell migration and chemotaxis, tissue development and repair, and leukocyte and tumor cell invasion.

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“…Muscle weakness and fatigue (hallmarks of MG) are functions of improper signaling between T-and B-cells which result in the elicitation of an antibody-mediated autoimmune response against the acetylcholine receptor (AChR) located at neuro-muscular junctions [2]. The mechanisms that contribute to the development or pathogenesis of MG are very complicated.…”

Section: Introductionmentioning

confidence: 99%

Altered let-7 expression in Myasthenia gravis and let-7c mediated regulation of IL-10 by directly targeting IL-10 in Jurkat cells

Jiang

Cheng

Qiu

et al. 2012

International Immunopharmacology

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Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms

Cited by 27 publications

References 35 publications

Neutralization of interleukin‐9 ameliorates symptoms of experimental autoimmune myasthenia gravis in rats by decreasing effector T cells and altering humoral responses

Neutralization of interleukin‐9 ameliorates symptoms of experimental autoimmune myasthenia gravis in rats by decreasing effector T cells and altering humoral responses

Functions of S100 Proteins

Altered let-7 expression in Myasthenia gravis and let-7c mediated regulation of IL-10 by directly targeting IL-10 in Jurkat cells

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