Retraction Note: Selected TLR7/8 agonist and type I interferon (IFN‑α) cooperatively redefine the microglia transcriptome

Khatun, Mst Reshma; Arifuzzaman, Sarder

doi:10.1007/s10787-020-00716-4

Cited by 2 publications

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“…The levels of CCL5 and CCL2, two major chemo-attractants of peripheral immune cells, were increased in MG6-1 microglia cells, cultured in the presence of IFN-β and TNFα [ 215 ], and in IFN-β-treated primary mouse microglia cultures [ 202 ]. Moreover, IFN-β and IFN-α enhanced the expression levels of TNF, IL-6, IL-1β, IL-1α, CXCL10, CXCL9 and NO in (LPS-stimulated) primary rodent microglia cultures [ 209 , 212 , 213 , 216 , 217 , 218 ] and microglia isolated after the maternal separation of the offspring of immune-activated dams [ 211 ]. Furthermore, the two interferons downregulated the levels of superoxide anions and glutamate [ 216 ], both related to neurotoxicity, and the IFN-β treatment of the primary cultures of microglia stimulated with DNA or RNA upregulated the expression of the members of the Pyrin and HIN200 domain-containing proteins (PYHIN) family of DNA sensors [ 219 ], all again pointing to an IFN-mediated switch towards a more pro-inflammatory microglia milieu.…”

Section: Molecular Effects Of Fda-approved Ms Drugs On Cns Cellsmentioning

confidence: 99%

“…In cultured microglia, more than in cultured astrocytes, IFN-α upregulated a wide set of genes related to pathogen detection and elimination, as well as a pro-inflammatory M1 phenotype [ 217 , 218 ]. Furthermore, the systemic administration of IFN-β to dams of a mouse maternal immune activation model increased the stress sensitivity of fetal microglia [ 211 ], showing its profound effect on this cell type.…”

Section: Molecular Effects Of Fda-approved Ms Drugs On Cns Cellsmentioning

confidence: 99%

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Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System

Kleijn

Martens

2020

IJMS

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Multiple sclerosis (MS) is characterized by peripheral and central inflammatory features, as well as demyelination and neurodegeneration. The available Food and Drug Administration (FDA)-approved drugs for MS have been designed to suppress the peripheral immune system. In addition, however, the effects of these drugs may be partially attributed to their influence on glial cells and neurons of the central nervous system (CNS). We here describe the molecular effects of the traditional and more recent FDA-approved MS drugs Fingolimod, Dimethyl Fumarate, Glatiramer Acetate, Interferon-β, Teriflunomide, Laquinimod, Natalizumab, Alemtuzumab and Ocrelizumab on microglia, astrocytes, neurons and oligodendrocytes. Furthermore, we point to a possible common molecular effect of these drugs, namely a key role for NFκB signaling, causing a switch from pro-inflammatory microglia and astrocytes to anti-inflammatory phenotypes of these CNS cell types that recently emerged as central players in MS pathogenesis. This notion argues for the need to further explore the molecular mechanisms underlying MS drug action.

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