Mast cells synthesize, store, and release nerve growth factor.

Leon, Alberta; Buriani, Alessandro; Toso, Roberto Dal; Fabris, Michele; Romanello, Stefano; Aloe, Luigi; Levi‐Montalcini, Rita

doi:10.1073/pnas.91.9.3739

Cited by 584 publications

(295 citation statements)

References 49 publications

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“…Several in vitro and in vivo studies published in the last few years have provided clear evidence that numerous cells of the immune system not only produce NGF (67,82,(114)(115)(116), but are also receptive to the action of NGF under both normal and pathologic conditions (21,45,66,117,118). The key in vivo observation suggesting an effect of NGF on these cells is that certain autoimmune inflammatory diseases are characterized by an activation of immunocytes and a significant alteration in the basal NGF levels.…”

Section: Ngf and Autoimmune Diseasesmentioning

confidence: 99%

“…MC can produce NGF (115), are receptive to the action of NGF (18,20,107), and can release numerous proinflammatory mediators, suggesting that NGF/MC interaction may be associated with inflammatory responses triggering homeostatie disregulation. Tlie fact that other forms of homeostatie alterations, such as aggressive behavior, stress induced by alcohol or heroin withdrawal, and parasitic infection, also result in an increase of circulating NGF (15, 123,124) suggests that NGF may be involved in mechanisms correlated with preventing and repairing possible damage to NGF target cells.…”

Section: Ngf and Autoimmune Diseasesmentioning

confidence: 99%

See 1 more Smart Citation

The expanding role of nerve growth factor: from neurotrophic activity to immunologic diseases

Aloe

Bracci-Laudiero

Бонини

et al. 1997

Allergy

204

127

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Numerous studies published in the last 10–15 years have shown that nerve growth factor (NGF), a polypeptide originally discovered in connection with its neurotrophic activity, also acts on cells of the immune system. NGF has been found in various immune organs including the spleen, lymph nodes, and thymus, and cells such as mast cells, eosinophils, and B and T cells. The circulating levels of NGF increase in inflammatory responses, in various autoimmune diseases, in parasitic infections, and in allergic diseases. Stress‐related events both in animal models and in man also result in an increase of NGF, suggesting that this molecule is involved in neuroendocrine functions. The rapid release of NGF is part of an alerting signal in response to either psychologically stressful or anxiogenic conditions in response to homeostatic alteration. Thus, the inflammation and stress‐induced increase in NGF might alone or in association with other biologic mediators induce the activation of immune cells during immunologic insults. A clearer understanding of the role of NGF in these events may be useful to identify the mechanisms implicated in certain neuroimmune and immune dysfunctions.

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Section: Ngf and Autoimmune Diseasesmentioning

confidence: 99%

Section: Ngf and Autoimmune Diseasesmentioning

confidence: 99%

The expanding role of nerve growth factor: from neurotrophic activity to immunologic diseases

Aloe

Bracci-Laudiero

Бонини

et al. 1997

Allergy

204

127

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“…[25][26][27][28] Among its pleiotropic effects, NGF induces platelet shape changes, 29 triggers monocyte cytotoxic activity, 22 and induces basophilic cell differentiation 30 -32 and mast cell development and degranulation. 24,33 However, NGF receptors have not been consistently detected on bone marrow cells. Although trkA and p75 LNGFR transcripts have been detected in long-term bone marrow cultures, 34,35 trkA transcripts were not always found within fresh bone marrow aspirates.…”

mentioning

confidence: 99%

Expression of Neurotrophins and their Receptors in Human Bone Marrow

Labouyrie

Dubus

Groppi

et al. 1999

The American Journal of Pathology

164

104

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The expression of neurotrophins and their receptors, the low-affinity nerve growth factor receptor (p75 LNGFR ) and the Trk receptors (TrkA , TrkB, and TrkC) , was investigated in human bone marrow from 16 weeks fetal age to adulthood. Using reverse transcription-polymerase chain reaction , all transcripts encoding for catalytic and truncated human TrkB or TrkC receptors were detected together with trkAI transcripts , whereas trkAII transcripts were found only in control nerve tissues. Transcripts for the homologue of the rat truncated TrkC(ic113) receptor were identified for the first time in human tissue. Stromal adventitial reticular cells were found immunoreactive for all neutrophin receptors. In contrast, hematopoietic cell types were not immunoreactive for p75 LNGFR Nerve growth factor (NGF) 1 is the prototype of a family of related neurotrophic factors known as neurotrophins (NT), which also includes brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4, also called neurotrophin-5 or NT-5 in humans) (reviewed in Lindsay et al 2 ). NT are trophic factors for the growth, differentiation, and survival of specific subsets of neurons in the developing and mature nervous system. 2 NT can interact with two classes of receptors with distinct ligand affinity and specificity. The low-affinity nerve growth factor receptor, p75 LNGFR , binds all known NT. 3,4 Tyrosine kinase receptors of the Trk family are essential components of NT high-affinity binding sites that trigger neuronal survival, growth, and differentiation. 5 TrkA is the preferred receptor for NGF 6,7 but has a lower efficiency for NT-3 or NT-4/5. TrkB is bound by BDNF and NT-4 and, to a lesser extent, by 9 TrkC is characterized by a unique ligand, NT-3. 10 In some cell lines, TrkA is sufficient to form high-affinity binding sites through homodimerization, 7 whereas p75 LNGFR potentiates TrkA activation by NGF in the PC12 cell line. 11 Variants of tyrosine kinase receptors (TK ϩ ) with insertions in either the extracellular domain (ECD) or the tyrosine kinase domain have been identified for trkA 12,13 and trkC [13][14][15][16] in both human and rat.Truncated receptors lacking the kinase domain (TK Ϫ ) have been described for TrkB and TrkC but not for TrkA. [15][16][17][18] These receptors may function as dominant negative isoforms or immunoadhesins. 13,19,20 Both TK ϩ and TK Ϫ receptors have been detected in neurons while only truncated TrkB and TrkC isoforms have been detected primarily in nonneuronal cells. [15][16][17][18]21 The expression of functional NGF receptors has been detected in several bone marrow-derived cells such as monocytes, 22 mastocytes, 23,24 and B or T cell clones. [25][26][27][28] Among its pleiotropic effects, NGF induces platelet shape changes, 29 triggers monocyte cytotoxic activity, 22 and induces basophilic cell differentiation 30 -32 and mast cell development and degranulation. 24,33 However, NGF receptors have not been consistently detected on bone marrow cells. Although trkA and p75 L...

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“…In the presence of interleukin-3 (IL-3) -secreting T cells rodent mast cell progenitors undergo proliferation and specific differentiation toward the mucosal phenotype [1][2][3][4][5], which is considered a major mechanism of defense during parasite infestation [6][7][8][9][10]. On the other hand, it is well established that both rodent and human mast cells are one main source for several cytokines [tumor necrosis factor ␣ (TNF-␣), IL-3, IL-4, IL-5, IL-6, IL-8, IL-13] [11][12][13][14][15][16][17][18][19] and growth factors [20,21] that can regulate directly or indirectly, the development, phenotype, and function of T [22][23][24][25][26][27][28] and B cells [21]. Subsequently, mast cells and T cells seem to complement the functions of each other, thus contributing to the cytokine pool that leads to chronic inflammation.…”

Section: Introductionmentioning

confidence: 99%