Crosstalks between the receptors tyrosine kinase EGFR and TrkA and the GPCR, FPR, in human monocytes are essential for receptors-mediated cell activation

Zein, Nabil El; D’Hondt, Stéphanie; Sariban, Eric

doi:10.1016/j.cellsig.2010.05.012

Cited by 41 publications

(33 citation statements)

References 51 publications

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“…Valente et al [73] found that the EGFRK activity of primary human monocytes mediated the up-regulation of CD14 by steroid ouabain. In accord with these observations, we have shown recently, for the first time, low-level EGFR expression on the surface of primary human peripheral blood monocytes [19], which has been confirmed subsequently [74]. Treatment with the cognate ligand EGF or infection with endothelial/monocyte tropic HCMV strains Towne/E or TB40/E phosphorylated EGFR within 10 min postinfection [19].…”

Section: Monocytes Exress Bona Fide Surface Egfr Which Is Activated supporting

confidence: 72%

Human cytomegalovirus induction of a unique signalsome during viral entry into monocytes mediates distinct functional changes: a strategy for viral dissemination

Chan

Nogalski

Stevenson

et al. 2012

Journal of Leukocyte Biology

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Review on the viral entry process of HCMV and the potential role of receptor-ligand interactions in modulating monocyte biology. HCMV pathogenesis is a direct consequence of the hematogenous dissemination of the virus to multiple host organ sites. The presence of infected monocytes in the peripheral blood and organs of individuals exhibiting primary HCMV infection have long suggested that these blood sentinels are responsible for mediating viral spread. Despite monocytes being “at the right place at the right time”, their short lifespan and the lack of productive viral infection in these cells complicate this scenario of a monocyte-driven approach to viral dissemination by HCMV. However, our laboratory has provided evidence that HCMV infection is able to induce a highly controlled polarization of monocytes toward a unique and long-lived proinflammatory macrophage, which we have demonstrated to be permissive for viral replication. These observations suggest that HCMV has evolved as a distinct mechanism to induce select proinflammatory characteristics that provide infected monocytes with the necessary tools to mediate viral spread following a primary infection. In the absence of viral gene products during the early stages of infection, the process by which HCMV “tunes” the inflammatory response in infected monocytes to promote viral spread and subsequently, viral persistence remains unclear. In this current review, we focus on the viral entry process of HCMV and the potential role of receptor-ligand interactions in modulating monocyte biology. Specifically, we examine the signaling pathways initiated by the distinct combination of cellular receptors simultaneously engaged and activated by HCMV during viral entry and how the acquisition of this distinct signalsome results in a nontraditional activation of monocytes leading to the induction of the unique, functional attributes observed in monocytes following HCMV infection.

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Section: Monocytes Exress Bona Fide Surface Egfr Which Is Activated supporting

confidence: 72%

Human cytomegalovirus induction of a unique signalsome during viral entry into monocytes mediates distinct functional changes: a strategy for viral dissemination

Chan

Nogalski

Stevenson

et al. 2012

Journal of Leukocyte Biology

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“…6, 7) could suggest that immune cells are activated in accordance with the following facts. TrkA expression in monocytes is associated with proinflammatory activity and production of reactive oxygen species [47]. TrkA acts as an inflammatory marker in monocytes/macrophages exposed to LPS and NGF [44].…”

Section: Discussionmentioning

confidence: 99%

Chronic Psychological Distress as an Inducer of Microglial Activation and Leukocyte Recruitment into the Area Postrema

Vargas-Caraveo

Pérez-Ishiwara

Martínez‐Martínez

2015

Neuroimmunomodulation

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Background: Chronic psychological distress can cause neuroinflammation, but the involvement of leukocytes in this inflammatory response remains unclear. The area postrema (AP) is considered a neural-immune interface because it lacks a blood-brain barrier and a site for leukocyte recruitment in neuroinflammatory conditions induced by immunological insults, but its role in chronic psychological distress has not been explored. Objective: To determine leukocyte recruitment to the AP after chronic psychological distress. Methods: Rats were exposed to cat odor for 5 consecutive days to induce distress, and, on the 6th day, their brains were dissected to perform immunohistofluorescence studies of the AP. Immune cells were identified and quantified with CD45 and CD11b markers. The distribution of neurons and immune cells was determined using TrkA and CD45 markers, respectively. Results: Distress induced a significant increase in CD45⁺ and CD11b⁺ cells in the AP. Three immunophenotypes were determined in the control and distress groups: CD45⁺/CD11b^-, CD45⁺/CD11b⁺ and CD45^-/CD11b⁺. CD expression, morphology and fluorescence intensity enabled the identification of different immune cell types: starting from longitudinal ramified microglia (mainly in the control group) to amoeboid microglia, monocytes and lymphocytes (mostly in the distressed group). TrkA and CD45 expression in the AP revealed the proximity between soma neurons and leukocytes. Interestingly, some CD45⁺ cells expressed TrkA, with increased expression in the distressed group. Conclusions: The identification of microglial activation, leukocyte recruitment and the close proximity between neurons and leukocytes in the AP after chronic psychological distress exposure suggests the AP as a site for distress-induced immune responses and engraftment of leukocytes infiltrating the CNS.

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“…47 There are several molecular techniques with variable specificities and sensitivities for detecting EGFR in oral mucosa and its association with various events in OSCC, (Table I). 3,9,17,19,20,27,28,31,34,35,38,39,41,45,47,48 The most widely used method for EGFR detection is IHC. It is a simple and relatively quick technique.…”

Section: Detection Methods Of Egfr In Oral Cancermentioning

confidence: 99%

“…Crosstalk between EGFR and other members of the ErbB family, cytokine receptors, ion channels, G protein-coupled receptors and various cell adhesion molecules has been described in the literature. 38,39 The integrin family phosphorylates the TK domain increasing the receptor activity. 40 Zein et al 38 studied the relationship that existed between the EGF-EGFR complexes and nerve growth factor with its receptor, finding that there is a bidirectional crosstalk between ligands and their receptors.…”

Section: Defects In Egfr Downregulationmentioning

confidence: 99%

“…38,39 The integrin family phosphorylates the TK domain increasing the receptor activity. 40 Zein et al 38 studied the relationship that existed between the EGF-EGFR complexes and nerve growth factor with its receptor, finding that there is a bidirectional crosstalk between ligands and their receptors. In HNC it has been observed that some of the ligands that bind to G protein-coupled receptors activate EGFR pathway, contributing to carcinogenesis.…”

Section: Defects In Egfr Downregulationmentioning

confidence: 99%

See 1 more Smart Citation

Dysregulation and detection methods of EGFR in oral cancer. A narrative review.

Somarriva

Fernández²,

Candia

et al. 2016

J Oral Res

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Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein, with an intracellular domain and tyrosine kinase function (TK) involved in cell proliferation. Dysfunctions in EGFR signaling pathways have been associated with oral malignant tumors such as oral squamous cell carcinoma (OSCC). Dysfunctions of EGFR may result from: increased EGF ligand; EGFR overexpression and copy number gain of the EGFR gene (EGFR CNG); EGFR mutations; failure in the downregulation of EGFR; and EGFR crosstalk. Of these alterations, overexpression of EGFR is by far the most studied dysfunction in OSCC. Clinicians should identify possible alterations of EGFR in the oral mucosa of patients, as EGFR can act as a biomarker for the diagnosis and prognosis of OSCC. Currently, there are several methods and techniques for detecting EGFR. Immunohistochemistry (IHC), fluorescence in situ hybridization (FISH) and polymerase chain reaction (PCR), are used to identify overexpression of EGFR, EGFR CNG and EGFR mutations, respectively. Detection of EGFR as a biomarker is key to identify any oral malignant transformation. Consequently, it becomes imperative to implement a non-invasive and inexpensive method of early diagnosis for OSCC in clinical practice.

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Crosstalks between the receptors tyrosine kinase EGFR and TrkA and the GPCR, FPR, in human monocytes are essential for receptors-mediated cell activation

Cited by 41 publications

References 51 publications

Human cytomegalovirus induction of a unique signalsome during viral entry into monocytes mediates distinct functional changes: a strategy for viral dissemination

Human cytomegalovirus induction of a unique signalsome during viral entry into monocytes mediates distinct functional changes: a strategy for viral dissemination

Chronic Psychological Distress as an Inducer of Microglial Activation and Leukocyte Recruitment into the Area Postrema

Dysregulation and detection methods of EGFR in oral cancer. A narrative review.

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