Search results for "Autoimmune"

Interleukin-9 and T helper type 9 cells in rheumatic diseases

2016

Summary Interleukin (IL)-9 is a 28-30 kDa monomeric glycosylated polypeptide belonging to the IL-7/IL-9 family of proteins that bind to a composite receptor consisting of the private receptor IL-9R and the IL-2 receptor, gamma (IL-2RG), a common gamma subunit shared by the receptors of many different cytokines. The IL-9R is expressed widely and IL-9 impacts a number of effector cells, such as effector T cells, B cells, innate lymphoid cells, mast cells, polymorphonuclear cells, epithelial cells and smooth muscle cells, playing an important role in regulating inflammatory immunity. The critical role of IL-9 in promoting cellular and humoral immune responses makes it an important focus of pot…

The Multiple Sclerosis Genomic Map: Role of peripheral immune cells and resident microglia in susceptibility

2017

Abstract:We assembled and analyzed genetic data of 47,351 multiple sclerosis (MS) subjects and 68,284 control subjects and establish a reference map of the genetic architecture of MS that includes 200 autosomal susceptibility variants outside the major histocompatibility complex (MHC), one chromosome X variant, and 32 independent associations within the extended MHC. We used an ensemble of methods to prioritize up to 551 potentially associated MS susceptibility genes, that implicate multiple innate and adaptive pathways distributed across the cellular components of the immune system. Using expression profiles from purified human microglia, we do find enrichment for MS genes in these brain -…

Cellular mechanisms of IL-17-induced blood-brain barrier disruption.

2009

Recently T-helper 17 (Th17) cells were demonstrated to disrupt the blood-brain barrier (BBB) by the action of IL-17A. The aim of the present study was to examine the mechanisms that underlie IL-17A-induced BBB breakdown. Barrier integrity was analyzed in the murine brain endothelial cell line bEnd.3 by measuring the electrical resistance values using electrical call impedance sensing technology. Furthermore, in-cell Western blots, fluorescence imaging, and monocyte adhesion and transendothelial migration assays were performed. Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice. IL-17A induced NADPH oxidase- or xanthine oxidase-dependent reactive oxygen species (ROS)…

Is molecular mimicry the culprit in the autoimmune haemolytic anaemia affecting patients with COVID‐19?

2020

Does dietary salt induce autoimmunity?

2013

Two recent publications suggest that dietary salt may polarize TH17 cells and therefore increase the risk of developing autoimmune disease. Where low salt diets can readily be tested for their therapeutic effects in autoimmune disease, more work is needed to connect dietary salts with the development of immunopathology.

Leukocyte migration test (LMT) in patients with thyroid disease: the response to human thyroid subcellular fractions.

1981

The response of circulating leukocytes to thyroid subcellular fractions was investigated in 19 patients with Graves' disease, 15 patients with Hashimoto's thyroiditis, 7 patients with toxic adenoma, 19 patients with nontoxic goiter and in 10 healthy students as control subjects. For this purpose, the leukocyte migration test of Soborg and Bendixen was performed against human crude thyroid extract (CTE), cell plasma membranes, nuclei, ribosomes, mitochondria and microsomes. Our results show positive LMT against: 1) CTE in patients with Graves' disease (61 +/- 13, p less than 0.001) and Hashimoto's thyroiditis (65 +/- 11, p less than 0.001) compared to controls (90 +/- 11); 2) cell plasma mem…

Genetic proof for the transient nature of the Th17 phenotype

2010

IL-17-producing CD4(+) T cells (Th17) have been classified as a new T helper cell subset. Using an IL-17 fate mapping mouse strain, which genetically fixes the memory of IL-17 expression, we demonstrate that IL-17A/F-expressing T helper cells generated either in vitro or in vivo are not a stable T-cell subset. Upon adoptive transfer of IL-17F-reporter-positive Th17 cells to RAG-deficient or WT animals, encephalitogenic Th17 cells partially lose IL-17 expression and upregulate IFN-γ. Additionally, we show that Th1 cells can convert in vivo to IL-17A/IFN-γ-coexpressing cells in the mesenteric lymph nodes (mLN). Our data classify IL-17A and IL-17F as cytokines produced transiently in response …

Lack of requirement for CD8+ cells in recovery from and resistance to experimental autoimmune encephalomyelitis.

1995

Abstract Experimental autoimmune encephalomyelitis (EAE) is a model of T-cell mediated autoimmune disease. Active disease is mediated by myelin basic protein specific CD4+T-cells, whose adoptive transfer can also induce passive disease. In the Lewis rat EAE is a transient disease inducing lasting resistance to rechallenge. The mechanisms of recovery and resistance are poorly understood. CD8+suppressor T-cells have mostly been thought to be central, especially in resistance to reinduction of the disease. In this study we showed by complete depletion of CD8+cells that this subset does not influence either recovery or resistance to EAE in the Lewis rat. This was further confirmed by depleting …

2014

Introduction We and others recently showed that IL-17-producing Th17 cells are highly unstable in their phenotype and swiftly upregulate T-bet and Th1-associated cytokines in the inflamed CNS of mice with EAE [1] . This inherent plasticity was recently associated with IL-23, IFN-γ or IL-12 signalling on effector T cells [2] , [3] . Aim To understand the role of IFN-γ and IL-27 signaling for plasticity of Th17 cells in vivo. Methods We use mice lacking the IFN-γ receptor 2 chain specifically in T cells (CD4cre × IFNγR2FL/FL) as well as blocking antibodies for IFN-γ and IL-27-p28 and knockout mice for IL-27-EBI3. Further we use IL-17 reporter mice to sort Th17 cells prior adoptive transfer. W…

Mesenchymal stem cells of Systemic Sclerosis patients, derived from different sources, show a profibrotic microRNA profiling

2019

AbstractSystemic Sclerosis (SSc) is a disease with limited therapeutic possibilities. Mesenchymal stem cells (MSCs)-therapy could be a promising therapeutic option, however the ideal MSCs source has not yet been found. To address this problem, we perform comparison between bone marrow (BM)-MSCs and adipose (A)-MSCs, by the miRs expression profile, to identify the gene modulation in these two MSCs source. MicroRNAs (miRs) are RNAs sequences, regulating gene expression and MSCs, derived from different tissues, may differently respond to the SSc microenvironment. The miRs array was used for the miRs profiling and by DIANA-mirPath tool we identified the biological functions of the dysregulated …