Abstract：
:Neurotrophins nerve growth factor (NGF), brain-derived growth factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4 (NT-4) and their high-affinity tyrosine protein kinase receptor (Trk) family, TrkA, TrkB, TrkC, and low-affinity p75(NTR) receptor, are key molecules implicated in the development of the central nervous system. Increasing evidence suggests that they also have physiological and pathological roles outside the nervous system. In this study we examined the expression of neurotrophins and their receptors in human activated macrophages and to what extent neurotrophins themselves modulate macrophage activation, in a model of primary adult monocyte-derived macrophage. Our data indicate that macrophages express neurotrophin and neurotrophin receptor genes differentially, and respond to cell stimulation by specific inductions. Neurotrophins did not modify the antigen-presenting capacities of macrophages or their production of proinflammatory cytokines, but somehow skewed their activation phenotype. In contrast, NGF clearly increased CXCR-4 expression in macrophage and their chemotactic response to low CXCL-12 concentration. The differential effect of specific macrophage stimuli on neurotrophin expression, in particular NGF and NT-3, and the specific enhancement of CXCR-4 expression suggest that neurotrophins might participate in tissue-healing mechanisms that should be investigated further in vivo.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
Samah B,Porcheray F,Gras Gdoi
10.1111/j.1365-2249.2007.03578.xsubject
Has Abstractpub_date
2008-03-01 00:00:00pages
476-86issue
3eissn
0009-9104issn
1365-2249pii
CEI3578journal_volume
151pub_type
杂志文章abstract：:Elevation of intracellular cAMP levels has been shown previously to inhibit cytokine secretion by various cell types in vitro. Since salmeterol is a beta 2-agonist which activates adenylate cyclase, its ability to inhibit cytokine production was evaluated. Though salmeterol, and the related drug albuterol, did not inh...
journal_title：Clinical and experimental immunology
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journal_title：Clinical and experimental immunology
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journal_title：Clinical and experimental immunology
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journal_title：Clinical and experimental immunology
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doi：
更新日期：1982-08-01 00:00:00
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journal_title：Clinical and experimental immunology
pub_type： 杂志文章
doi：
更新日期：1988-11-01 00:00:00
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journal_title：Clinical and experimental immunology
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doi：
更新日期：1987-08-01 00:00:00
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journal_title：Clinical and experimental immunology
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doi：
更新日期：1979-07-01 00:00:00
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journal_title：Clinical and experimental immunology
pub_type： 杂志文章
doi：10.1111/j.1365-2249.1993.tb06003.x
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journal_title：Clinical and experimental immunology
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更新日期：1988-10-01 00:00:00
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journal_title：Clinical and experimental immunology
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更新日期：1989-01-01 00:00:00
abstract：:Different genetic mutations have been described in complement component C7 deficiency, a molecular defect which is clinically associated with an increased susceptibility to neisserial recurrent infections, although some cases remain asymptomatic. In this work we report the genetic bases of C7 deficiency in one Spanish...
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