Implication of the MAPK pathways in the maturation of human dendritic cells induced by nickel and TNF-?

Boislevé, Fanny; Kerdine-Römer, Saadia; Pallardy, Marc

doi:10.1016/j.tox.2004.08.015

Cited by 82 publications

(63 citation statements)

References 37 publications

(54 reference statements)

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“…Overall the cellular responses of immune cells, including DCs triggered with a wide variety of stimuli, are often suggested to involve extensive cross-talk between PI3K-AKT, PKC, and MAPK signaling cascades (45)(46)(47)(48). In this perspective, TLR2 and NOD receptor-driven maturation of human DCs involved NOTCH1-PI3K-PKC␦-dependent activation of ERK1/2 and p38 MAPK.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to NOTCH signaling, a diverse set of signaling events, including the PI3K/AKT and MAPK pathways, as well as the active heterodimer p50/p65 form of nuclear factor-B (NF-B), have been suggested to play a central role in maturation of DCs by inducing expression of a variety of genes involved in maturation processes (45)(46)(47)(48). In this regard, engagement of TLR2 and NOD receptors triggered the activation of the PI3K pathway under CTLA-4-or TGF-␤-triggered immunosuppressive conditions as evaluated by phosphorylation status of p85, GSK-3␤, and 4EBP1 (Figs.…”

Section: Notch1-pi3k Signaling Dynamics Integrated Into Signaling Cohmentioning

confidence: 99%

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Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation

Ghorpade

Kaveri

Bayry

et al. 2011

Journal of Biological Chemistry

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Dendritic cells (DCs) as sentinels of the immune system are important for eliciting both primary and secondary immune responses to a plethora of microbial pathogens. Cooperative stimulation of a complex set of pattern-recognition receptors, including TLR2 and nucleotide-binding oligomerization domain (NOD)-like receptors on DCs, acts as a rate-limiting factor in determining the initiation and mounting of the robust immune response. It underscores the need for "decoding" these multiple receptor interactions. In this study, we demonstrate that TLR2 and NOD receptors cooperatively regulate functional maturation of human DCs. Intriguingly, synergistic stimulation of TLR2 and NOD receptors renders enhanced refractoriness to TGF-␤-or CTLA-4-mediated impairment of human DC maturation. Signaling perturbation data suggest that NOTCH1-PI3K signaling dynamics assume critical importance in TLR2-and NOD receptor-mediated surmounting of CTLA-4-and TGF-␤-suppressed maturation of human DCs. Interestingly, the NOTCH1-PI3K signaling axis holds the capacity to regulate DC functions by virtue of PKC␦-MAPK-dependent activation of NF-B. This study provides mechanistic and functional insights into TLR2-and NOD receptor-mediated regulation of DC functions and unravels NOTCH1-PI3K as a signaling cohort for TLR2 and NOD receptors. These findings serve in building a conceptual foundation for the design of improved strategies for adjuvants and immunotherapies against infectious diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Notch1-pi3k Signaling Dynamics Integrated Into Signaling Cohmentioning

confidence: 99%

Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation

Ghorpade

Kaveri

Bayry

et al. 2011

Journal of Biological Chemistry

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“…Recent studies also showed that p38 MAPK is activated by NiSO 4 in human monocytederived DC and cooperates for IL-12 production (Antonios et al, 2010). In human CD34 + -derived DC, nickel activates p38 MAPK, ERK1/2 and JNK, all of which are MAPKs involved in the expression of CD83, CD86 and CCR7 but not in the nickel-induced down-regulation of E-cadherin and Langerin (Boisleve et al, 2005). TNF-α production induced by DNCB was also linked to the activation of p38 MAPK and JNK (Boisleve et al, 2004).…”

Section: Activation Of the Mitogen-activated Protein Kinases (Mapks)mentioning

confidence: 99%

“…Different signalling pathways such as MAPKs and NF-kB play important roles in DC maturation (Rescigno et al, 1998;Arrighi et al, 2001;Aiba et al, 2003;Boisleve et al, 2005;Neves et al, 2009). The MAPKs p38 MAPK and extracellular signal-regulated kinases 1/2 (ERK1/2) are involved in a wide variety of cellular responses, including proliferation, differentiation and apoptosis.…”

Section: Activation Of the Mitogen-activated Protein Kinases (Mapks)mentioning

confidence: 99%

“…Various immune responses in dendritic cells are positively regulated by NF-kB, such as the production of inflammatory mediators, cytokines/chemokines and the up-regulation of surface molecules (Kaisho and Tanaka, 2008). In addition, the NF-kB signalling pathway is reported to be involved in DC maturation (Rescigno et al, 1998;Arrighi et al, 2001;Aiba et al, 2003;Boisleve et al, 2005;Neves et al, 2009). Indeed some of the phenotypic and functional changes induced in DC by haptens are dependent upon the activation of NF-kB.…”

Section: Activation Of the Nf-kb Transcription Factormentioning

confidence: 99%

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Signal transduction profile of chemical sensitisers in dendritic cells: An endpoint to be included in a cell-based in vitro alternative approach to hazard identification?

Neves

Gonçalo

Figueiredo

et al. 2011

Toxicology and Applied Pharmacology

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The development of non-animal testing methods for the assessment of skin sensitisation potential is an urgent challenge within the framework of existing and forthcoming legislation. Efforts have been made to replace current animal tests, but so far no alternative methods have been developed. It is widely recognised that alternatives to animal testing cannot be accomplished with a single approach, but rather will require the integration of results obtained from different in vitro and in silico assays. The argument subjacent to the development of in vitro dendritic cell (DC)-based assays is that sensitiser-induced changes in the DC phenotype can be differentiated from those induced by irritants. This assumption is derived from the unique capacity of DC to convert environmental signals encountered at the skin into a receptor expression pattern (MHC class II molecules, co-stimulatory molecules, chemokine receptors) and a soluble mediator release profile that will stimulate T lymphocytes. Since signal transduction cascades precede changes in surface marker expression and cytokine/ chemokine secretion, these phenotypic modifications are a consequence of a signal transduction profile that is specifically triggered by sensitisers and not by irritants. A limited number of studies have addressed this subject and the present review attempts to summarise and highlight all of the signalling pathways modulated by skin sensitisers and irritants. Furthermore, we conclude this review by focusing on the most promising strategies suitable for inclusion into a cell-based in vitro alternative approach to hazard identification.

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Contact sensitizers downregulate the expression of the chemokine receptors CCR6 and CXCR4 in a skin dendritic cell line

Cruz

Gonçalo

Paiva³

et al. 2005

Arch Dermatol Res

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Chemokines are involved in the control of dendritic cell (DC) trafficking, which is critical for the immune response, namely in allergic contact dermatitis (ACD). In this work, we investigated by flow cytometry the effect of the contact sensitizers 2,4-dinitrofluorobenzene (DNFB), 1,4-phenylenediamine (PPD) and nickel sulfate (NiSO 4 ), on the surface expression of the chemokine receptors CCR6 and CXCR4 in DC. As an experimental model of a DC we used a fetal skin-derived dendritic cell line (FSDC), which has morphological, phenotypical and functional characteristics of skin DC. Our results show that all the skin sensitizers studied decreased the membrane expression of the chemokine receptors CCR6 and CXCR4. In contrast, 2,4-dichloronitrobenzene (DCNB), the inactive analogue of DNFB without contact sensitizing properties, was without effect on the surface expression of these receptors. Lipopolysaccharide (LPS), which induces the maturation of DC, also reduced surface CCR6 and CXCR4 expression.

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Implication of the MAPK pathways in the maturation of human dendritic cells induced by nickel and TNF-?

Cited by 82 publications

References 37 publications

Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation

Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation

Signal transduction profile of chemical sensitisers in dendritic cells: An endpoint to be included in a cell-based in vitro alternative approach to hazard identification?

Contact sensitizers downregulate the expression of the chemokine receptors CCR6 and CXCR4 in a skin dendritic cell line

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