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61.
A cross-regulation between type I IFN and TNFα has been proposed recently, where both cytokines are hypothesized to counteract
each other. According to this model, different autoimmune diseases can be viewed as disequilibrium between both cytokines.
As this model may have important clinical implications, the present review summarizes and discusses the currently available
clinical evidence arguing for or against the proposed cross-regulation between TNFα and type I IFN. In addition, we review
how this cross-regulation works at the cellular and molecular levels. Finally, we discuss the clinical relevance of this proposed
cross-regulation for biological therapies such as type I IFN or anti-TNFα treatment. 相似文献
62.
Lisa GM van Baarsen Carla A Wijbrandts François Rustenburg Tineke Cantaert Tineke CTM van der Pouw Kraan Dominique L Baeten Ben AC Dijkmans Paul P Tak Cornelis L Verweij 《Arthritis research & therapy》2010,12(1):R11
Introduction
Cross-regulation between TNF and type I IFN has been postulated to play an important role in autoimmune diseases. Therefore, we determined the effect of TNF blockade in rheumatoid arthritis (RA) on the type I IFN response gene activity in relation to clinical response. 相似文献63.
In a recent paper written by Hilbe et al (BMC vet res, 2009), the nature and specificity of the prion protein deposition in
the kidney of feline species affected with feline spongiform encephalopathy (FSE) were clearly considered doubtful. This article
was brought to our attention because we published several years ago an immunodetection of abnormal prion protein in the kidney
of a cheetah affected with FSE. At this time we were convinced of its specificity but without having all the possibilities
to demonstrate it. As previously published by another group, the presence of abnormal prion protein in some renal glomeruli
in domestic cats affected with FSE is indeed generally considered as doubtful mainly because of low intensity detected in
this organ and because control kidneys from safe animals present also a weak prion immunolabelling. Here we come back on these
studies and thought it would be helpful to relay our last data to the readers of BMC Vet res for future reference on this
subject. 相似文献
64.
在研究转基因香石竹品系月之霓裳(Moonshade)、月之伊人(Moonlite)中外源基因F3’5’H的表达中,本文克隆了F3’5’H全长基因1.5kb,构建获得工程菌株Escherichia coli BL21(DE3)(+F3'5'H)。SDS-PAGE分析的结果显示,该菌株高效表达出F3’5’H重组蛋白,约占菌体总蛋白的30%。用经纯化的F3’5’H重组蛋白作为抗原,制备F3’5’H重组蛋白的抗血清,经ELISA免疫学分析表明,该抗血清的效价为1:25600。Western blot结果表明F3’5’H重组蛋白具有良好的IgG结合活性,且抗血清与转基因香石竹品系月之霓裳和月之伊人中的外源基因F3’5’H所表达的蛋白发生明显的抗原抗体反应。这样,月之霓裳和月之伊人用于评价转基因香石竹品系的环境安全性在我国也得到了验证。 相似文献
65.
Alexandre Wagner Silva de Souza Johanna Westra Johan Bijzet Pieter C Limburg Coen A Stegeman Marc Bijl Cees GM Kallenberg 《Arthritis research & therapy》2013,15(5):R104
Background
Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are systemic inflammatory disorders that include granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), Churg-Strauss syndrome and renal limited vasculitis (RLV). Extracellular high-mobility group box 1 (HMGB1) acts as an alarmin and has been shown to be a biomarker of disease activity as well as an autoantigen in systemic lupus erythematosus (SLE) and, possibly, in AAV. This study aims to assess antibodies against HMGB1 and HMGB1 levels as biomarkers for AAV disease activity and predictors of relapsing disease.Methods
AAV patients with active disease and healthy controls (HC) were evaluated for anti-HMGB1 antibodies while serum HMGB1 levels were measured longitudinally in AAV patients at presentation, during remission, prior to and at relapses.Results
HMGB1 levels were similar between AAV patients at presentation (n = 52) and HC (n = 35) (2.64 ± 1.80 ng/ml vs. 2.39 ± 1.09 ng/ml; P = 0.422) and no difference regarding HMGB1 levels could be found among AAV disease subsets (GPA: 2.66 ± 1.83 ng/ml vs. MPA: 3.11 ± 1.91 ng/ml vs. RLV: 1.92 ± 1.48 ng/ml; P = 0.369). AAV patients with renal involvement had lower HMGB1 levels than patients without renal involvement at presentation (2.35 ± 1.48 ng/ml vs. 3.52 ± 2.41 ng/ml; P = 0.042). A negative correlation was observed between HMGB1 levels and 24-hour proteinuria (ρ = -0.361, P = 0.028). Forty-nine AAV patients were evaluated for HMGB1 levels during follow-up and no differences were observed between relapsing and nonrelapsing patients (P = 0.350). No significant increase in HMGB1 levels was observed prior to a relapse compared with the remission period and changes in HMGB1 levels were not associated with an increased risk for relapse in AAV. Positivity for anti-HMGB1 antibodies was low in patients with active AAV (three out of 24 patients).Conclusions
Serum HMGB1 levels at presentation are not increased and are lower in patients with renal involvement. Relapses are not preceded or accompanied by significant rises in HMGB1 levels and changes in HMGB1 levels are not related to ensuing relapses. Anti-HMGB1 antibodies are present in only a few patients in AAV. In contrast to SLE, HMGB1 is not a useful biomarker in AAV. 相似文献66.
Sofieke E Klamer Carlijn GM Kuijk Peter L Hordijk C Ellen van der Schoot Marieke von Lindern Paula B van Hennik Carlijn Voermans 《Cell Adhesion & Migration》2013,7(5):434-449
Cell adhesion and migration are important determinants of homing and development of hematopoietic stem and progenitor cells (HSPCs) in bone marrow (BM) niches. The extracellular matrix protein transforming growth factor-β (TGF-β) inducible gene H3 (BIGH3) is involved in adhesion and migration, although the effect of BIGH3 is highly cell type-dependent. BIGH3 is abundantly expressed by mesenchymal stromal cells, while its expression in HSPCs is relatively low unless induced by certain BM stressors. Here, we set out to determine how BIGH3 modulates HSPC adhesion and migration. We show that primary HSPCs adhere to BIGH3-coated substrates, which is, in part, integrin-dependent. Overexpression of BIGH3 in HSPCs and HL60 cells reduced the adhesion to the substrate fibronectin in adhesion assays, which was even more profound in electrical cell-substrate impedance sensing (ECIS) assays. Accordingly, the CXCL12 induced migration over fibronectin-coated surface was reduced in BIGH3-expressing HSPCs. The integrin expression profile of HSPCs was not altered upon BIGH3 expression. Although expression of BIGH3 did not alter actin polymerization in response to CXCL12, it inhibited the PMA-induced activation of the small GTPase RAC1 as well as the phosphorylation and activation of extracellular-regulated kinases (ERKs). Reduced activation of ERK and RAC1 may be responsible for the inhibition of cell adhesion and migration by BIGH3 in HSPCs. Induced BIGH3 expression upon BM stress may contribute to the regulation of BM homeostasis. 相似文献
67.
Reina JA de Kinderen Danielle AJE Lambrechts Debby Postulart Alfons GH Kessels Jos GM Hendriksen Albert P Aldenkamp Marian HJM Majoie 《BMC neurology》2011,11(1):10
Background
Epilepsy is a neurological disorder, characterized by recurrent unprovoked seizures which have a high impact on the individual as well as on society as a whole. In addition to the economic burden, epilepsy imposes a substantial burden on the patients and their surroundings. Patients with uncontrolled epilepsy depend heavily on informal care and on health care professionals. About 30% of patients suffer from drug-resistant epilepsy. The ketogenic diet can be a treatment of last resort, especially for children. The beneficial effect of the ketogenic diet has been proven, but information is lacking about its cost-effectiveness. In the current study we will evaluate the (cost-) effectiveness of the ketogenic diet in children and adolescents with intractable epilepsy. 相似文献68.
Dolff S Abdulahad WH Westra J Doornbos-van der Meer B Limburg PC Kallenberg CG Bijl M 《Arthritis research & therapy》2011,13(5):R157
Introduction
Systemic lupus erythematosus (SLE) is an autoimmune disease accompanied by a disturbed T-cell balance skewed towards effector T-cells, in particular Th17-cells. The novel cytokine interleukin-21 (IL-21) is suggested to be crucial for triggering T-cell responses towards IL-17 producing cells. Thus, we aimed to investigate the ability of T-cells to produce IL-21 and IL-17 in SLE patients. 相似文献69.
Banderali U Belke D Singh A Jayanthan A Giles WR Narendran A 《Cellular physiology and biochemistry》2011,28(6):1169-1180
Acute Myeloid Leukemia (AML) accounts for approximately one fifth of all childhood leukemia yet is responsible for a significant proportion of morbidity and mortality in this population. For this reason, research to identify novel targets for the development of effective AML therapeutics has intensified in the recent past. The THP-1 cell line, which was originally established from an infant diagnosed with AML, provides an experimental model for functional, pre-clinical therapeutics and target identification studies of AML. Here we show the expression of the voltage gated potassium channel Kv11.1 in THP-1 cells as opposed to normal hematopoietic stem cells. In addition, curcumin, a natural polyphenol derived from the plant Curcuma longa, effectively blocked Kv11.1 activity and also inhibited the proliferation of these cells. Curcumin was rapidly internalized by THP-1 cells and possibly exerts potential growth inhibitory activity by interacting with intracellular epitopes of the ion channel. Inhibition of ionic currents carried by Kv11.1 resulted in depolarization of cell membrane potential. We propose that the inhibition of Kv11.1 activity by curcumin may lead to interference with leukemic cell physiology and consequently the suppression of survival and proliferation of AML cells. 相似文献
70.
Urine levels of HMGB1 in Systemic Lupus Erythematosus patients with and without renal manifestations
Deena A Abdulahad Johanna Westra Johannes Bijzet Sebastian Dolff Marcory C van Dijk Pieter C Limburg Cees GM Kallenberg Marc Bijl 《Arthritis research & therapy》2012,14(4):R184