Endogenous NGF affects monocyte antigen presentation (Abstract/Comunicazione in atti di convegno)

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Label
  • Endogenous NGF affects monocyte antigen presentation (Abstract/Comunicazione in atti di convegno) (literal)
Anno
  • 2005-01-01T00:00:00+01:00 (literal)
Alternative label
  • Bracci Laudiero L (1); Aloe L (1); Caroleo MC (2); Buanne P (3); Costa N (4); Starace G (1); Lundeberg T (5) (2005)
    Endogenous NGF affects monocyte antigen presentation
    in 6th Meeting of the International Society of NeuroImmunoModulation, Atene, Grecia, 25-28 Settembre 2005
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Bracci Laudiero L (1); Aloe L (1); Caroleo MC (2); Buanne P (3); Costa N (4); Starace G (1); Lundeberg T (5) (literal)
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Note
  • Abstract (literal)
  • Comunicazione (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1) Istituto di Neurobiologia e Medicina Molecolare 2) Universita' di Calabria, Cosenza 3) Universita' de L Aquila, L'Aquila 4) Universita' della Magna Grecia, Catanzaro 5) Karolinska Hospital, Stockholm, Sweden (literal)
Titolo
  • Endogenous NGF affects monocyte antigen presentation (literal)
Abstract
  • A growing number of studies on inflammatory diseases have demonstrated that the inflammatory state is characterised by up-regulation of Nerve Growth Factor (NGF) synthesis. In addition, purified immune cells involved in innate and acquired immunity show a basal expression of NGF, whose synthesis is enhanced after stimulation with specific antigens and cytokines. In spite of the large number of studies, it is still not clear why NGF is produced in vivo during the inflammation process and how its local synthesis, often in an autocrine fashion, can influence the ongoing immune response. We recently showed that the autocrine NGF synthesis in B-lymphocytes directly regulates the expression and release in these cells of calcitonin gene-related peptide (CGRP), a neuropeptide able to inhibit immune response, suggesting a possible NGF anti-inflammatory action. To test this hypothesis we investigated whether endogenous NGF can regulate the synthesis of CGRP in monocytes and how the autocrine synthesis of either NGF or CGRP can influence monocyte functions. For this study we used human monocytes purified from buffy-coats by Percoll gradients and immunomagnetic negative selection and cultured in the presence or absence of 100ng/ml LPS, with or without the addition of 100ng/mlNGF or 10?g/ml neutralizing anti-NGF antibodies or isotypic IgG or CGRP8-37. CGRP expression was analyzed by RT-PCR, immunofluorescence and flow cytometry analysis. Our results showed that monocytes synthesise basal levels of CGRP and after LPS stimulation, CGRP expression is up-regulated. Endogenous NGF production, induced in monocytes by LPS stimulation, regulates CGRP synthesis. Using neutralizing anti-NGF antibodies, the expression of CGRP decreases in resting cells and the up-regulation of CGRP induced by LPS is prevented. The neutralization of endogenous NGF significantly enhances CD86 and HLA-DR expression while reducing IL-10 synthesis, and functionally affects antigen presentation as observed in the allogeneic mixed leukocyte reaction. Similar but not identical effects were observed when endogenous CGRP action was blocked by using CGRP8-37, the CGRP receptor I antagonist. Taken together our results show that the endogenous synthesis of NGF in monocytes has a functional role and by reducing the antigen presenting capacity and co-stimulatory function of monocytes NGF can dampen the immune response. (literal)
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