Impact of α-defensins1–3 on the maturation and differentiation of human monocyte-derived DCs. Concentration-dependent opposite dual effects

Rodriguez-García, Marta; Oliva, Harold; Climent, Núria; Escribese, María M.; García, Felipe; Moran, Thomas M.; Gatell, José M.; Gallart, Teresa

doi:10.1016/j.clim.2009.01.012

Cited by 22 publications

(26 citation statements)

References 39 publications

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“…Indeed, antimicrobial molecules such as LL-37, lactoferrin, and a-defensins can inhibit DC activation (33,54,56,57). In addition, elastase can induce TGF-b (32) and reduce proinflammatory cytokine production by moDC, thus promoting CD4 + lymphocyte T regulatory polarization (31).…”

Section: Discussionmentioning

confidence: 99%

“…Activated PMN can promote DC migration (28) and also modulate DC maturation and activation through cell-cell contacts (29), ectosome release (30), or mediator secretion. Interestingly, several granule-derived mediators such as lactoferrin, LL-37, calprotectins, a-defensins, elastase, bactericidal/permeability-increasing protein, MPO, and proteinase 3 have been shown to either downregulate (31)(32)(33)(34)(35)(36)(37) or upregulate (33,(38)(39)(40)(41)) DC functions, depending on the study.…”

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confidence: 99%

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Neutrophil Extracellular Traps Downregulate Lipopolysaccharide-Induced Activation of Monocyte-Derived Dendritic Cells

Barrientos

Bignon

Gueguen

et al. 2014

The Journal of Immunology

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Polymorphonuclear neutrophils (PMN) play a central role in inflammation and participate in its control, notably by modulating dendritic cell (DC) functions via soluble mediators or cell–cell contacts. Neutrophil extracellular traps (NETs) released by PMN could play a role in this context. To evaluate NET effects on DC maturation, we developed a model based on monocyte-derived DC (moDC) and calibrated NETs isolated from fresh human PMN. We found that isolated NETs alone had no discernable effect on moDC. In contrast, they downregulated LPS-induced moDC maturation, as shown by decreased surface expression of HLA-DR, CD80, CD83, and CD86, and by downregulated cytokine production (TNF-α, IL-6, IL-12, IL-23), with no increase in the expression of tolerogenic DC genes. Moreover, the presence of NETs during moDC maturation diminished the capacity of these moDC to induce T lymphocyte proliferation in both autologous and allogeneic conditions, and modulated CD4+ T lymphocyte polarization by promoting the production of Th2 cytokines (IL-5 and IL-13) and reducing that of Th1 and Th17 cytokines (IFN-γ and IL-17). Interestingly, the expression and activities of the lymphoid chemokine receptors CCR7 and CXCR4 on moDC were not altered when moDC matured in the presence of NETs. Together, these findings reveal a new role for NETs in adaptive immune responses, modulating some moDC functions and thereby participating in the control of inflammation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Neutrophil Extracellular Traps Downregulate Lipopolysaccharide-Induced Activation of Monocyte-Derived Dendritic Cells

Barrientos

Bignon

Gueguen

et al. 2014

The Journal of Immunology

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“…human hBD-3 and HNP-1 to -3, can initiate the maturation of DCs, up-regulate the expression of co-stimulatory molecules and activate professional antigen-presenting cells [27,28]. Interestingly, it has been demonstrated that effects on DCs mediated by the defensins HNP-1 to -3 are typically observed with low concentrations of defensins that do not have direct antimicrobial activity [28]. This observation also aligns with the recent paradigm that the anti-infective mechanism mediated by some HDPs is largely due to the modulation of host immunity.…”

Section: Diverse Immunity-related Biological Effectsmentioning

confidence: 99%

Cationic Host Defence Peptides: Multifaceted Role in Immune Modulation and Inflammation

2012

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Host defence peptides (HDPs) are innate immune effector molecules found in diverse species. HDPs exhibit a wide range of functions ranging from direct antimicrobial properties to immunomodulatory effects. Research in the last decade has demonstrated that HDPs are critical effectors of both innate and adaptive immunity. Various studies have hypothesized that the antimicrobial property of certain HDPs may be largely due to their immunomodulatory functions. Mechanistic studies revealed that the role of HDPs in immunity is very complex and involves various receptors, signalling pathways and transcription factors. This review will focus on the multiple functions of HDPs in immunity and inflammation, with special reference to cathelicidins, e.g. LL-37, certain defensins and novel synthetic innate defence regulator peptides. We also discuss emerging concepts of specific HDPs in immune-mediated inflammatory diseases, including the potential use of cationic peptides as therapeutics for immune-mediated inflammatory disorders.

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“…[20][21][22] Moreover, immature (im) MD-DC from healthy individuals produce α-defensins1-3 23 and α-defensins1-3 are able to modulate the maturation and differentiation process of MD-DC. 24 A high production of α-defensins 1-3 by immature DC could act by damaging the virus prior or after its internalization. This would favor a more efficient viral processing and presentation to CD4 + T cells with a minor rate of infectious HIV transmission.…”

Section: Myeloid-derived Dendritic Cells (Md-dc) As a Cellular Adjuvamentioning

confidence: 99%

Dendritic cell based vaccines for HIV infection

García

Plana

Climent

et al. 2013

Human Vaccines & Immunotherapeutics

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Impact of α-defensins1–3 on the maturation and differentiation of human monocyte-derived DCs. Concentration-dependent opposite dual effects

Cited by 22 publications

References 39 publications

Neutrophil Extracellular Traps Downregulate Lipopolysaccharide-Induced Activation of Monocyte-Derived Dendritic Cells

Neutrophil Extracellular Traps Downregulate Lipopolysaccharide-Induced Activation of Monocyte-Derived Dendritic Cells

Cationic Host Defence Peptides: Multifaceted Role in Immune Modulation and Inflammation

Dendritic cell based vaccines for HIV infection

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