Turnover and kinetics of epidermal langerhans cells and their dendritic precursor cells in experimental contact dermatitis

Kolde, G.

doi:10.1007/bf02505224

Cited by 6 publications

(3 citation statements)

References 36 publications

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“…A similar decreased migration of immature DC in the presence of conditioned media of HPV16 VLP-treated keratinocytes was also observed, suggesting that viral particles could also affect the intra-epithelial recruitment of LC precursors [33] (data not shown).…”

Section: Discussionsupporting

confidence: 56%

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

Herman¹,

Hubert²,

Herfs³

et al. 2010

Eur J Immunol

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Human papillomavirus (HPV) infection, particularly type 16, is causally associated with cancer of the uterine cervix. The progression of cervical lesions suggests that viral antigens are not adequately presented to the immune system. The aim of this study was to determine whether HPV16 viral particles can influence the trafficking of human DC/ Langerhans cells (LC), either by direct interactions with DC or following incubation with human normal keratinocytes that are in close contact with LC in the squamous epithelium. We first demonstrated that HPV16 L1 major capsid protein, when self-assembled into virus-like particles (VLP), is able to induce in DC an over-expression of CXC receptor 4 (CXCR4) via the activation of the NF-jB signaling pathway and to enhance DC motility in the presence of CXCL12, suggesting an ability to migrate towards lymph nodes. We also showed that conditioned media of HPV16 VLP-treated keratinocytes induce a lower LC migration than those from untreated keratinocytes and that prostaglandin E2 (PGE 2 ), detected in HPV16 VLP-treated keratinocyte supernatants, may reduce LC recruitment into the squamous epithelium. Taken together, our data demonstrate that HPV16 VLP may differentially regulate the immune protective response according to their target cells.Key words: APC . Cell trafficking . Chemokines . HPV16 VLP Supporting Information available online IntroductionMore than 90% of cervical cancers and precursor lesions (squamous intraepithelial lesions, SIL) may be attributed to the infection by oncogenic types of human papillomavirus (HPV) [1]. However, HPV alone is not sufficient for tumor progression [2]. Additional environmental and/or host factors are probably involved in malignant progression as suggested by the small proportion of infected individuals developing cervical cancer and the relatively long latency period before cancer emergence [3]. The importance of the immune system in the control of HPV infection and lesion development is shown, indirectly, by the high Eur. J. Immunol. 2010. 40: 3075-3084 DOI 10.1002 Immunity to infection 3075 prevalence and persistence of HPV infections in immunosuppressed individuals [4] and by the fact that an increased cellular immune response is correlated with a good clinical prognosis [5]. The DC lineage is a family of professional APC. On exposure to danger signals such as pathogens, immature DC are able to process antigens and to mature through a dramatic change in their cell surface markers [6]. The migration of maturing DC to the draining lymph nodes results in the interactions between DC and naive T cells and in the initiation of an antigen-specific immune response [7]. Furthermore, the signals induced within draining lymph nodes can cause the expansion of lymphatic vessels, sustaining and amplifying the effective homing of DC [8]. Indeed, migration of DC from the site of antigen capture to secondary lymphoid organs is a crucial event in the initiation and amplification of immune responses. In turn, inflammatory sites can recruit circulating...

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Section: Discussionsupporting

confidence: 56%

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

Herman¹,

Hubert²,

Herfs³

et al. 2010

Eur J Immunol

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“…IFN-Á, released by CD8+ effector cells in contact dermatitis, induces keratinocytes to upregulate their Fas expression [26]. In addition, CTL can kill Langerhans cells, which are known to undergo apoptotic cell death in contact hypersensitivity [27]. The cell death of epidermal cells carrying a hapten, caused by these CTL killing mechanisms, in turn, may favor the release, upon lethal hit, of a wide array of inflammatory cytokines and chemokines [25], responsible both for the cutaneous inflammation and for the clinical picture of allergic contact dermatitis/contact hypersensitivity [28].…”

Section: Molecular Killing Mechanismsmentioning

confidence: 99%

The Immunology of Contact Dermatitis

Markert

Elsner²

2003

Exog Dermatol

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Contact dermatitis can be induced by a variety of small antigens. After binding of such antigens to a skin protein, they form a hapten-protein complex which can be incorporated into Langerhans cells or which can develop intracellularly. These complexes or their fragments can be presented via major histocompatibility complex (MHC) II by professional antigen-presenting cells or via MHC I by any cell present in the skin. The following activation of cytotoxic CD8+ T cells induces death of the presenting cell, including Langerhans cells or keratinocytes, which leads to an enormous release of immunoactive and chemoattractant cytokines and chemokines, initiating a strong inflammation.

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“…In fact, interferon γ, released by CD8‐positive effector cells in ACD, causes keratinocytes to upregulate their Fas expression 64 . In addition, CTL can kill Langerhans cells, which are known to undergo apoptotic cell death in CHS 66 . The cell death of epidermal cells carrying a hapten, caused by these CTL killing mechanisms, in turn, may favour the release, upon lethal hit, of a wide array of inflammatory cytokines and chemokines, 65 responsible both for the cutaneous inflammation and for the clinical picture of ACD/CHS 67 …”

Section: The Central Role Of Molecular Killingmechanisms In Allergic mentioning

confidence: 99%

Alterations in molecular killing mechanisms: implications in skin disease

Panfilis

2001

Br J Dermatol

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Cytolytic T lymphocytes exert two main specific molecular killing mechanisms against target cells, namely (i) they can synthesize and release soluble cytolytic factors, and (ii) they can express effector molecules that act as ligands of receptors expressed by target cells on the cell surface; by these two pathways cytolytic T lymphocytes kill several targets, e.g. cells infected with intracellular pathogens, cells transformed by malignancy and cells producing autoantibodies. This review investigates the contribution from alterations in these molecular killing mechanisms to the pathogenesis of cutaneous diseases. In fact, molecular components involved in such killing mechanisms are often altered or distorted in skin pathology, e.g. cutaneous viral infections, skin cancer, contact hypersensitivity and autoimmune diseases with cutaneous involvement. Treatments capable of repairing the molecular components operating in such killing mechanisms could presumably favour the resolution of these skin diseases.

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Turnover and kinetics of epidermal langerhans cells and their dendritic precursor cells in experimental contact dermatitis

Cited by 6 publications

References 36 publications

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

The Immunology of Contact Dermatitis

Alterations in molecular killing mechanisms: implications in skin disease

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