2012
DOI: 10.1016/j.jneuroim.2012.07.018
|View full text |Cite
|
Sign up to set email alerts
|

Theiler's murine encephalomyelitis virus induced phenotype switch of microglia in vitro

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

2
25
0

Year Published

2015
2015
2023
2023

Publication Types

Select...
9

Relationship

1
8

Authors

Journals

citations
Cited by 24 publications
(27 citation statements)
references
References 66 publications
2
25
0
Order By: Relevance
“…Immunohistochemistry was performed as described 67 , 68 . Briefly, formalin-fixed, paraffin-embedded tissue sections were treated with 0.5% H 2 O 2 to block endogenous peroxidase, depending on the antibody heated in sodium citrate buffer, and incubated with 20% goat serum to block non-specific binding sites.…”
Section: Methodsmentioning
confidence: 99%
“…Immunohistochemistry was performed as described 67 , 68 . Briefly, formalin-fixed, paraffin-embedded tissue sections were treated with 0.5% H 2 O 2 to block endogenous peroxidase, depending on the antibody heated in sodium citrate buffer, and incubated with 20% goat serum to block non-specific binding sites.…”
Section: Methodsmentioning
confidence: 99%
“…Ribonucleic acid (RNA) was isolated from frozen brain and spinal cord tissue using the RNeasy Lipid Tissue Mini Kit (Qiagen, Hilden, Germany) and subsequently transcribed into cDNA with the Omniscript RT Kit (Qiagen), Random Primers (Promega, Mannheim, Germany), and RNase Out (Invitrogen, Darmstadt, Germany). RT-qPCR was performed for TMEV, IL-1β, IL-6, IL-17, IL-34, Csf1r, TNFα, IFNγ, TGFβ1, and three housekeeping genes (GAPDH, β-Actin, HPRT) using standard protocols, the Mx3005P qPCR System (Agilent Technologies Deutschland GmbH, Böblingen, Germany), and Brilliant III Ultra-Fast SYBR®QPCR Master Mixes (Gerhauser et al, 2005(Gerhauser et al, , 2012. Forward (F) and reverse (R) primers designed for TMEV and murine genes were as follows: TMEV-F 5′-GACTAATCAGAGGAACGTCAGC-3′, TMEV-R 5′-GTGAAGAGCGGCAAGTGAGA-3′; IL-1β-F 5′-AGCTACCTGTGTCTTT CCCG-3′, IL-1β-R 5′-AGTGCAGTTGTCTAATGGGAAC-3′; IL-6-F 5′-GTT CTCTGGGAAATCGTGGA-3′, IL-6R 5′-CCAGAGGAAATTTTCAATA GGC-3′; IL-17-F 5′-ACTCTCCACCGCAATGAAGA-3′, IL-17R 5′-CTCTCA GGCTCCCTCTTCAG-3′; IL-34-F 5′-GCCACCTTTGCTGACCTAAG-3′, IL-34R 5′-TTTCCCAAAGCCACGTCAAG-3′; Csf1r-F 5′-AGGAGGTGACAGT GGTTGAG-3′, Csf1r-R 5′-CATGGTCTTGCACACGTAGG-3′; TNFα-F 5′-GCCTCTTCTCATTCCTGCTT-3′, TNFα-R 5′-CACTTGGTGGTTTGCTA CGA-3′; IFNγ-F 5′-CACGGCACAGTCATTGAAAG-3′, IFNγ-R 5′-AATCTG GCTCTGCAGGATTT-3′; TGFβ1-F 5′-TTGCTTCAGCTCCACAGAGA-3′, TGFβ1-R 5′-TGGTTGTAGAGGGCAAGGAC-3′.…”
Section: Rt-qpcrmentioning
confidence: 99%
“…Finally, models of viral-induced demyelination are used to study the spontaneous development of inflammatory demyelination in the CNS in the absence of the active (and artificial) induction of an antigen-specific autoimmune response (Gerhauser et al 2012). The pathogenesis of these models, however, is highly complex, involving direct viral-induced damage of brain cells or oligodendrocytes, a complex immune response involving MHC class I and II-restricted T cells, and potentially pathogenic antibodies against viral proteins or even autoantigens.…”
Section: Microglia In Preclinical Studiesmentioning
confidence: 99%