Showing papers in "Journal of Neuroimmunology in 2007"

TL;DR: The role of specific cell types including leukocytes, endothelium, glia, microglia, the extracellular matrix and neurons, and mediators produced by inflammatory cells such as cytokines, chemokines, reactive oxygen species and arachidonic acid metabolites are reviewed.

TL;DR: While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate APP processing by upregulation of beta secretase 1 and therefore are able to establish a vicious cycle.

TL;DR: It is shown here that TLR2-deficient mice develop a decreased CNS injury compared to wild type mice in a model of focal cerebral ischemia and concludes thatTLR2 in microglia propagates stroke-induced CNS injury.

TL;DR: The disease PLOSL and the finding that TREM2 of microglia is required for tissue debris clearance provide prototypic molecular evidence that dysfunctional innate immunity can be disease causative leading to a chronic neurodegenerative process.

TL;DR: Analyzing Treg from AD and PD patients as well as non-affected individuals revealed that the frequency of Treg (CD4(+)Foxp3(+)) increases with age and is accompanied by intensified suppressive activity for Treg in patients.

TL;DR: Data suggest that modulation of TLR4 signaling may attenuate ischemic injury in hippocampal neurons and activate ischemia-induced hippocampal neuronal death.

TL;DR: The role of axonal loss early in disease or during relapsing-remitting disease is still under investigation, as are the interactions and interdependency between inflammation, demyelination, neurodegeneration and neuroprotection in the pathogenesis of MS.

TL;DR: It is demonstrated that interactions between PD-1/PD-L1, but not PD- 1/PDL-2, are crucial in attenuating T cell responses in EAE.

TL;DR: A role of glutamate as a key immunomodulator in the initiation and development of T-cell-mediated immunity in peripheral tissues as well as in the central nervous system is suggested.

TL;DR: There is increasing evidence that a specific T cell subpopulation, namely T helper cells type 2 (Th2 cells) are particularly beneficial in the context of CNS lesions, and investigating the potential of a systemic Th2 shift to improve outcome after CNS injury is extremely promising.

TL;DR: It is demonstrated that anti-NAE autoantibodies, in addition to anti-thyroid autoant ibodies, are emphasized as useful serological diagnostic markers of HE.

TL;DR: It is concluded that IFNbeta-1a therapy enhances T(Reg) function, and this may be relevant in the inflammatory environment of MS lesions, and the ex vivo and in vitro effects of IFNâ- 1a (Rebif) on regulatory T-cell function are evaluated.

TL;DR: This study suggests that CCL19 plays a role in both the physiological immunosurveillance of the healthy CNS and the pathological maintenance of immune cells in the CNS of MS patients.

TL;DR: It is suspected that autoantibodies arising from peripheral B cells bind to aquaporin 4 expressed on astrocyte foot processes on the abluminal surface of microvessels, activate complement and initiate inflammatory demyelination and necrosis in NMO.

TL;DR: The presence of antibody specificity to GD1a/GD1b and/or GD1b/GT1b was significantly associated with severe disability and a requirement for mechanical ventilation in anti-GSC-positive GBS patients.

TL;DR: Results showed that BALB/c mice peritoneal macrophages express a functional subset of GABA(A)R subunits, which significantly reduced their in vitro production of IL-6 and IL-12 after GABA adding to the culture medium.

TL;DR: The studies suggest that LXR agonists suppress the production of pro-inflammatory molecules by CNS glia, at least in part, by modulating NF-kappaB-signaling pathways.

TL;DR: It is reported that MP4-induced EAE displays characteristic differences in CNS pathology as compared to MOG peptide 35-55-elicited disease, including dynamic and stage-dependent shifting from the brain to the spinal cord and finally to the cerebellum.

TL;DR: Generated autoantibodies against major etiopathogenic molecular targets as neuroimmune markers of dementia were measured by ELISA in patient sera and may be used as a differential biomarker profile in designing AD therapeutic strategies involving early vaccination.

TL;DR: Specific astrocyte binding of anti-TPO aAb suggests a role of these aAb in the HE pathogenesis, and in immunofluorescence assays on monkey brain cerebellum sections, both HE patients' sera and anti- TPO monoclonal antibodies (mAb) were able to bind cerebellar cells expressing glial fibrillary acid protein.

TL;DR: S100B was able to stimulate IL-6 and TNF-alpha secretion in cultured astrocytes in a concentration- and time-dependent manner as shown by ELISA and the subcellular localization of RAGE expression at the cell surface membrane of cultured Astrocytes was demonstrated.

TL;DR: In this article, a total of 105 consecutive multiple sclerosis (MS) patients were divided into 52 opticospinal MS (OSMS) and 53 conventional MS (CMS), and their sera along with those from 85 healthy controls (HC) were examined by an enzyme-linked immunosorbent assay using antibodies against H. pylori.

TL;DR: It is demonstrated that T cells isolated from lymph nodes and spleens of Cop-1 immunized animals protect the nigrostriatal system from MPTP-induced neurodegeneration in a dose-dependent manner and further support the use of immunomodulatory strategies for Parkinson's disease.

TL;DR: Experimental evidence strongly supports the concept that inflammation in MS is aimed not only at destroying and phagocytosing damaged cells but also at promoting tissue regeneration or tissue repair via scar formation through resolution or protective phase.

TL;DR: Ex vivo and in vitro observations imply that the Th1 lineage is more encephalitogenic than is suggested by adoptive transfer of Th1 (IL-17-/IFN-gamma+) cell lines which have been terminally differentiated in vitro.

TL;DR: A variety of mitochondrion-driven mechanisms involved in immune regulation, oligodendrocyte depletion and neurodegeneration are discussed, highlighting the importance of an early aggressive intervention for halting inflammation and preventing neurodegenersation and identifying the mitochondrions as a potential target in neuroprotection.

TL;DR: The manner in which inflammation in the CNS contributes to, and protects against, neurodegeneration is considered, in a review of the recent human disease and animal model literature.

TL;DR: It is concluded that CCI causes PMN invasion of the DRG whereby the functional implication of their close proximity to neuronal axon and soma remains unknown.

TL;DR: The results suggest that short-term reduced circulating Tregs may be associated with the pathogenesis of two subtypes of GBS, including monophasic self-limiting course in GBS.

TL;DR: Existing data from different gene expression profiling studies that have been conducted in multiple sclerosis and EAE are summarized, potential problems are discussed and future directions for the use of microarrays in MS are proposed.