TLR3 impairment in human newborns

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00179906%3A_____%2F13%3A10196506" target="_blank" >RIV/00179906:_____/13:10196506 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11150/13:10196506
Result on the web
<a href="http://dx.doi.org/10.1189/jlb.1212617" target="_blank" >http://dx.doi.org/10.1189/jlb.1212617</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1189/jlb.1212617" target="_blank" >10.1189/jlb.1212617</a>

Result language
angličtina
Original language name
TLR3 impairment in human newborns
Original language description
Newborns are highly susceptible to viral infections. We hypothesized that this susceptibility could be due to a dysregulated expression of innate virus-sensing receptors, i.e., TLR3, TLR7, TLR8, and TLR9 and the cytosolic receptors retinoic acid-inducible gene I, melanoma differentiation-associated protein 5, protein kinase R, and IFN-gamma-inducible protein 16. Cord blood mononuclear cells (CBMCs) expressed mRNA for all these receptors except for TLR3. In peripheral blood mononuclear cells (PBMCs), TLR3 mRNA was preferentially expressed in cytotoxic cells, particularly CD56(dim) NK cells. Cord NK cells in contrast showed low TLR3 mRNA expression and lacked TLR3 protein expression. Cord NK cells did not produce IFN-gamma in response to polyinosinic-polycytidylic acid [poly(I:C)], whereas strong IFN-gamma production was observed in poly(I:C)-stimulated adult NK cells. Cord NK cells had poor cytotoxic function that was only marginally enhanced by exposure to the TLR3 ligand poly(I:C). Op
Czech name
—
Czech description
—

Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FK - Gynaecology and obstetrics
OECD FORD branch
—

Publication year
2013
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Similar results(10)