RT info:eu-repo/semantics/article
T1 Stimulation of FcγR receptors induces monocyte chemoattractant protein-1 in the human monocytic cell line THP-1 by a mechanism involving IκB-α degradation and formation of p50/p65 NF-κB/Rel complexes
A1 Alonso, Andrés
A1 Bayón Prieto, Yolanda
A1 Renedo, Marta
A1 Sánchez Crespo, Mariano
K1 Chemokines
K1 Fc receptors
K1 Monocytes
K1 Macrophages
K1 Quimiocinas
K1 Monocitos
K1 Macrófagos
K1 24 Ciencias de la Vida
AB THP-1 monocytic/macrophage cells were stimulated via their FcγR receptors with insolubleaggregates of human IgG and the production of the C–C chemokine monocyte chemoattractantprotein (MCP)-1 assayed. A dose- and time-dependent production of MCP-1 comparable to thatproduced by the most potent agonists could be detected in the culture medium by a sensitiveELISA assay. This was accompanied by a parallel activation of the transcription factor NF-κBasjudged from both the appearance ofκB-binding activity containing p50/p65 NF-κB/Rel complexes inthe nuclear extract and the disappearance of the NF-κB inhibitor IκB-αin the cell lysate. Incontrast, IκB-βand IκB-εexpression was not modified, thus pointing to the occurrence of aselective degradation of IκB-αunder those conditions. Attempts to modulate MCP-1 productionwith compounds that display inhibitory effects on the activation of NF-κB such as the proteasomeinhibitorN-acetyl-leucinyl-leucinyl-norleucinal, the antioxidant pyrrolidine dithiocarbamate and thesalicylate derivative 2-hydroxy-4-trifluoromethylbenzoic acid showed a parallel effect on bothMCP-1 production and NF-κB activation, thus pointing to the involvement ofκB-binding sites onthe transcriptional regulation of MCP-1 production. Our findings suggest the existence inmonocytic cells of a signaling mechanism initiated by cross-linking of low-affinity FcγR, most likelyof the FcγRII family since THP-1 cells do not express FcγRIII receptors, that involves activation ofNF-κB associated to the proteolytic degradation of IκB-αand leads to the transcriptional up-regulation of MCP-1
PB Oxford University Press
SN 0953-8178
YR 2000
FD 2000
LK https://uvadoc.uva.es/handle/10324/47500
UL https://uvadoc.uva.es/handle/10324/47500
LA eng
NO International Immunology, 2000, vol. 12, n. 4, p. 547-554
NO Producción Científica
DS UVaDOC
RD 24-nov-2024