http://www.cnr.it/ontology/cnr/individuo/prodotto/ID4282
Human monocyte/macrophages activate by exposure to LPS overexpress NGF and NGF receptors. (Articolo in rivista)
- Type
- Label
- Human monocyte/macrophages activate by exposure to LPS overexpress NGF and NGF receptors. (Articolo in rivista) (literal)
- Anno
- 2001-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/S0165-5728(00)00441-0 (literal)
- Alternative label
Caroleo M.C. (1), Costa N. (2), Bracci-Laudiero L. (3), Aloe L (3). (2001)
Human monocyte/macrophages activate by exposure to LPS overexpress NGF and NGF receptors.
in Journal of neuroimmunology (Print); Elsevier, New York (Stati Uniti d'America)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Caroleo M.C. (1), Costa N. (2), Bracci-Laudiero L. (3), Aloe L (3). (literal)
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- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- (1)Faculty of Pharmacy, Department of Pharmacobiology, University of Calabria,
Cosenza, Italy.
(2) Faculty of Pharmacy, University of Magna Grecia, Catanzaro, Italy
(3) Institute of Neurobiology, CNR, Rome Italy (literal)
- Titolo
- Human monocyte/macrophages activate by exposure to LPS overexpress NGF and NGF receptors. (literal)
- Abstract
- Monocyte/macrophages (M/M) represent the main cellular component of the immune
system involved in the inflammatory response. In the present study we investigate
whether NGF is produced by M/M and is involved in this event. The results show
that unstimulated human M/M produce NGF and its synthesis is stimulated by LPS.
The increase of NGF is associated with enhanced expression of high affinity NGF
receptor on M/M and with no changes of low affinity NGF receptors (p75). The
neutralization of endogenous NGF by NGF antibody in LPS-activated M/M, leads to
overexpression of p75 receptor causing apoptosis. These findings provide new
insight in the mechanisms governing monocyte survival in the inflamed tissue,
representing a crucial aspect of host defence and maintenance of homeostasis. (literal)
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