scholarly journals Keratinocytes from human skin respond as typical immune cells after the stimulation with Trichophyton rubrum

2007 ◽  
Author(s):  
Alfonso Islas-Rodríguez ◽  
Luz García-Madrid
Keyword(s):  
Human Skin ◽  
Immune Cells ◽  
Trichophyton Rubrum

Labeling and tracking of immune cells in ex vivo human skin

2020 ◽  
Author(s):  
Feline E. Dijkgraaf ◽  
Mireille Toebes ◽  
Mark Hoogenboezem ◽  
Marjolijn Mertz ◽  
David W. Vredevoogd ◽  
...  
Keyword(s):  
Human Skin ◽  
Immune Cells ◽  
Ex Vivo

Number of Langerhans immune cells in painful and non-painful human skin after shingles

2003 ◽  
Vol 294 (12) ◽  
pp. 529-535 ◽  
Author(s):  
Anne Oaklander ◽  
Adelaine E. Stocks ◽  
Peter R. Mouton
Keyword(s):  
Human Skin ◽  
Immune Cells

scholarly journals Measles skin rash: infection of lymphoid and myeloid cells in the dermis precedes viral dissemination to keratinocytes in the epidermis

2019 ◽  
Author(s):  
Brigitta M. Laksono ◽  
Paola Fortugno ◽  
Bernadien M. Nijmeijer ◽  
Rory D. de Vries ◽  
Sonia Cordisco ◽  
...  
Keyword(s):  
Human Skin ◽  
Skin Rash ◽  
Immune Cells ◽  
Ex Vivo ◽  
Myeloid Cells ◽  
Lateral Spread ◽  
Epidermal Keratinocytes ◽  
Viral Dissemination ◽  
Combining Data ◽  
Infected Cells

AbstractMeasles is characterised by fever and a maculopapular skin rash, which is associated with immune clearance of measles virus (MV)-infected cells. Histopathological analyses of skin biopsies from humans and non-human primates (NHPs) with measles rash have identified MV-infected keratinocytes and mononuclear cells in the epidermis, around hair follicles and near sebaceous glands. Here, we address the pathogenesis of measles skin rash by combining data from experimentally infected NHPs, ex vivo infection of human skin sheets and in vitro infection of primary human keratinocytes. Longitudinal analysis of the skin of experimentally MV-infected NHPs demonstrated that infection in the skin precedes onset of rash by several days. MV infection was initiated in lymphoid and myeloid cells in the dermis before dissemination to the epidermal keratinocytes. These data were in good concordance with ex vivo MV infections of human skin sheets, in which dermal cells were more targeted than the epidermal ones. To address viral dissemination to the epidermis and to determine whether the dissemination is receptor-dependent, we performed experimental infections of primary keratinocytes collected from healthy or nectin-4-deficient donors. These experiments demonstrated that MV infection of keratinocytes is nectin-4-dependent, and nectin-4 expression was higher in differentiated than in proliferating keratinocytes. Based on these data, we hypothesise that measles skin rash is initiated by migrating MV-infected lymphocytes that infect dermal skin-resident CD150+ immune cells. The infection is subsequently disseminated from the dermal papillae to nectin-4+ keratinocytes in the basal epidermis. Lateral spread of MV infection is observed in the superficial epidermis, most likely due to the higher level of nectin-4 expression on differentiated keratinocytes. Finally, MV-infected cells are cleared by infiltrating immune cells, causing hyperaemia and oedema, which give the appearance of morbilliform skin rash.Author SummarySeveral viral infections are associated with skin rash, including parvovirus B19, human herpesvirus type 6, dengue virus and rubella virus. However, the archetype virus infection that leads to skin rash is measles. Although all of these viral exanthemata often appear similar, their pathogenesis is different. In the case of measles, the appearance of skin rash is a sign that the immune system is clearing MV-infected cells from the skin. How the virus reaches the skin and is locally disseminated remains unknown. Here we combine observations and expertise from pathologists, dermatologists, virologists and immunologists to delineate the pathogenesis of measles skin rash. We show that MV infection of dermal myeloid and lymphoid cells precedes viral dissemination to the epidermal keratinocytes. We speculate that immune-mediated clearance of these infected cells results in hyperaemia and oedema, explaining the redness of the skin and the slightly elevated spots of the morbilliform rash.

scholarly journals Development of humanized mouse and rat models with full-thickness human skin and autologous immune cells

2020 ◽  
Author(s):  
Yash Agarwal ◽  
Cole Beatty ◽  
Sara Ho ◽  
Lance Thurlow ◽  
Antu Das ◽  
...  
Keyword(s):  
Human Skin ◽  
Immune Cells ◽  
Immune Cell ◽  
Lymphoid Tissues ◽  
Rodent Models ◽  
Full Thickness ◽  
Human Pathogens ◽  
Major Barrier ◽  
Rat Models ◽  
Route Of Infection

AbstractThe human skin is a major barrier for host defense against many human pathogens, with several pathogens directly targeting the skin for replication and disease. The skin is also the primary route of infection for a myriad of vector-borne diseases; thus cutaneous immune cells play a major role in modulating transmission for such infectious diseases. Several human pathogens that target the skin as a major route of infection are unable to infect traditional rodent models or recapitulate the pathogenesis in humans. It is well established that differences exist in human skin and immune cell biology compared to rodent models. Therefore, rodent (mouse and rat) models that incorporate human skin and immune cells would addressed the above discussed technical gap, and enable in vivo mechanistic studies of human host-skin pathogen interactions, and support the development of novel therapeutics. Here, we introduce the novel human Skin and Immune System (hSIS)-humanized NOD-scid IL2Rgnull (NSG) mouse and Sprague-Dawley-Rag2tm2hera Il2rgtm1hera (SRG) rat models, co-engrafted with full-thickness human fetal skin, autologous fetal lymphoid tissues, and fetal liver-derived hematopoietic stem cells. hSIS-humanized rodents support the development of adult-like, full-thickness human skin and human lymphoid tissues, and support human immune cell development. Furthermore, the engrafted human skin supports Methicillin-resistant Staphylococcus aureus infection, demonstrating the utility of these humanized rodent models in studying human disease.

scholarly journals RIG-I Activation by a Designer Short RNA Ligand Protects Human Immune Cells against Dengue Virus Infection without Causing Cytotoxicity

2019 ◽  
Vol 93 (14) ◽  
Author(s):  
Victor Ho ◽  
Hui Yee Yong ◽  
Marion Chevrier ◽  
Vipin Narang ◽  
Josephine Lum ◽  
...  
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Human Skin ◽  
Immune Cells ◽  
Viral Infections ◽  
Short Hairpin Rna ◽  
Dengue Virus Infection ◽  
Hairpin Rna ◽  
Short Hairpin ◽  
Rna Ligands

ABSTRACT Virus-derived double-stranded RNA (dsRNA) molecules containing a triphosphate group at the 5′ end are natural ligands of retinoic acid-inducible gene I (RIG-I). The cellular pathways and proteins induced by RIG-I are an essential part of the innate immune response against viral infections. Starting from a previously published RNA scaffold (3p10L), we characterized an optimized small dsRNA hairpin (called 3p10LG9, 25 nucleotides [nt] in length) as a highly efficient RIG-I activator. Dengue virus (DENV) infection in cell lines and primary human skin cells could be prevented and restricted through 3p10LG9-mediated activation of RIG‐I. This antiviral effect was RIG-I and interferon signal dependent. The effect was temporary and was reversed above a saturating concentration of RIG-I ligand. This finding revealed an effective feedback loop that controls potentially damaging inflammatory effects of the RIG-I response, at least in immune cells. Our results show that the small RIG-I activator 3p10LG9 can confer short-term protection against DENV and can be further explored as an antiviral treatment in humans. IMPORTANCE Short hairpin RNA ligands that activate RIG-I induce antiviral responses in infected cells and prevent or control viral infections. Here, we characterized a new short hairpin RNA molecule with high efficacy in antiviral gene activation and showed that this molecule is able to control dengue virus infection. We demonstrate how structural modifications of minimal RNA ligands can lead to increased potency and a wider window of RIG-I-activating concentrations before regulatory mechanisms kick in at high concentrations. We also show that minimal RNA ligands induce an effective antiviral response in human skin dendritic cells and macrophages, which are the target cells of initial infection after the mosquito releases virus into the skin. Using short hairpin RNA as RIG-I ligands could therefore be explored as antiviral therapy.

scholarly journals Development of humanized mouse and rat models with full-thickness human skin and autologous immune cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yash Agarwal ◽  
Cole Beatty ◽  
Sara Ho ◽  
Lance Thurlow ◽  
Antu Das ◽  
...  
Keyword(s):  
Human Skin ◽  
Immune Cells ◽  
Full Thickness ◽  
Humanized Mouse ◽  
Rat Models

scholarly journals Author Correction: Development of humanized mouse and rat models with full-thickness human skin and autologous immune cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yash Agarwal ◽  
Cole Beatty ◽  
Sara Ho ◽  
Lance Thurlow ◽  
Antu Das ◽  
...  
Keyword(s):  
Human Skin ◽  
Immune Cells ◽  
Full Thickness ◽  
Humanized Mouse ◽  
Rat Models

scholarly journals Histopathological Findings of Trichophyton rubrum Infection in Ex vivo Human Skin

2020 ◽  
pp. 42-44
Author(s):  
Hyun Ji Lee ◽  
Chihyeon Sohng ◽  
Jun Young Kim ◽  
Kyung Duck Park ◽  
Seok-Jong Lee ◽  
...  
Keyword(s):  
Human Skin ◽  
Trichophyton Rubrum ◽  
Ex Vivo ◽  
Histopathological Findings
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