In: Journal of Neurology, 2015, vol. 262, no. 4, p. 870-880
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In: Journal of Neurology, 2015, vol. 262, no. 8, p. 1909-1917
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In: Schizophrenia Bulletin, 2017, vol. 43, no. 3, p. 493-496
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In: Pathogens, 2020, vol. 9, no. 1, p. 21
Microglia are the chief immune cells of the brain and have been reported to be activated in severe malaria. Their activation may drive towards neuroinflammation in cerebral malaria. Malaria-infected red blood cell derived-extracellular vesicles (MiREVs) are produced during the blood stage of malaria infection. They mediate intercellular communication and immune regulation, among other...
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In: Nature communications, 2017, vol. 8, p. 1600
We have previously reported the molecular signature of murine pathogenic TH17 cells that induce experimental autoimmune encephalomyelitis (EAE) in animals. Here we show that human peripheral blood IFN-γ+IL-17+ (TH1/17) and IFN-γ−IL-17+ (TH17) CD4+ T cells display distinct transcriptional profiles in high-throughput transcription analyses. Compared to TH17 cells, TH1/17 cells have gene...
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In: Scientific Reports, 2019, vol. 9, no. 1, p. 10603
Forebrain glial cells - ependymal cells and astrocytes -acquire upon injury- a “reactive” phenotype associated with parvalbumin (PV) upregulation. Since free radicals, e.g. reactive oxygen species (ROS) play a role in the pathogenesis of multiple sclerosis, and that PV-upregulation in glial cells is inversely correlated with the level of oxidative stress, we hypothesized that...
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In: Plos one, 2011, vol. 6, no. 6, p. e21386
FoxP3+ Treg cells are believed to play a role in the occurrence of autoimmunity and in the determination of clinical recurrences. Contradictory reports are, however, available describing frequency and function of Treg cells during autoimmune diseases. We examined, by both polychromatic flow cytometry, and real-time RT-PCR, several Treg markers in peripheral blood mononuclear cells from...
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In: Frontiers in immunology, 2018, vol. 9, p. 2118
Chemokine synergy-inducing molecules are emerging as regulating factors in cell migration. The alarmin HMGB1, in its reduced form, can complex with CXCL12 enhancing its activity on monocytes via the chemokine receptor CXCR4, while the form containing a disulfide bond, by binding to TLR2 or TLR4, initiates a cascade of events leading to production of cytokines and chemokines. So far, the...
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In: Acta Neuropathologica, 2014, vol. 128, no. 2, p. 231-246
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In: Cancer Causes & Control, 2014, vol. 25, no. 3, p. 395-403
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