Virus recovery from brain cultures of mice infected with either Semliki Forest and/or Langat depended on the time interval between inoculation of either virus. Mixed infections may alter the course of a disease.
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Suppression of neuroinflammation by an allosteric agonist and positive allosteric modulator of the α7 nicotinic acetylcholine receptor GAT107.
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Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah University Hospital and Hebrew University Medical School, Jerusalem, Israel.
Background: The α7 nicotinic acetylcholine receptor (α7 nAChR) negatively regulates the synthesis and release of pro-inflammatory cytokines by immune cells. Our previous studies showed that in encephalitogenic T cells, α7 nAChR expression is upregulated and that activation of the cholinergic system can attenuate experimental autoimmune encephalomyelitis (EAE). GAT107 is an allosteric agonist and positive allosteric modulator (ago-PAM) of α7 nAChR that can produce persistent activation of this receptor.
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Flaviviruses are zoonotic encephalitogenic pathogens of humans and animals that are transmitted by arthropod vectors. Effective vaccines against all but the yellow fever virus and the Japanese encephalitis virus among flaviviruses have eluded the persistent efforts of researchers. CD8+ cytotoxic T lymphocytes play a critical role in control of intracellular pathogens and hence are expected to contribute significantly to protection against flavivirus disease, while their ability to destroy infected neurons is bound to result in damage to the central nervous system (CNS).
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Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease of the central nervous system (CNS) in young adults. Chronic treatments with histone deacetylase inhibitors (HDACis) have been reported to ameliorate experimental autoimmune encephalomyelitis (EAE), a rodent model of MS, by targeting immune responses. We have recently shown that the HDAC inhibition/knockdown in the presence of thyroid hormone (T3) can also promote oligodendrocyte (OL) differentiation and expression of myelin genes in neural stem cells (NSCs) and oligodendrocyte precursors (OPCs).
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