LCs maintain skin immune surveillance and are involved in skin disorders, including psoriasis … The variability of the LC response to viral infection may be contributed to by different cell types being infected by the virus, differences in viral life cycle and gene expression in those cells, whether the LCs themselves are infected, and whether the virus has direct immune modifying effects on the LCs. LC precursors are located to the epidermis from the lamina propria/basal membrane via BMP7‐ALK3 signaling, whereas differentiation in the mucosa is dependent on transforming growth factor beta1 and ALK5.17. Epicutaneous immunization has also been used to convert an established Th1 response to a Th2 response through reduction of Th1 cytokines,85 and LC‐like DCs are able to be stimulated with an adjuvant to direct the development of Th1 and Th2 cells in vivo.133 If this were also the case for LCs, they could potentially be used to skew responses to either a Th1 or Th2 in the skin, which would have application for immunomodulation of Th1‐dominant diseases such as AD. Langerhans cells are dendritic but unpigmented and are found nearer the skin surface than melanocytes. Symptoms of Langerhans cell histiocytosis based on the organ affected include: Increased LC numbers have been observed in the wound edge of human diabetic foot ulcers, while reduced numbers were found in the newly formed epidermis, using CD207/langerin immunohistochemical staining.116 LC density has also been associated with healing outcomes in human diabetic foot ulcers,117 where healing ulcers had an increased number of LCs at the wound edge than nonhealing ulcers. Use the link below to share a full-text version of this article with your friends and colleagues. Inhibition of this pathway restores the upregulation of costimulatory marker expression and the response to the viral antigen.28, LCs are also suppressed by HPV in other ways. Human epidermal Langerhans cells maintain immune homeostasis in skin by activating skin resident regulatory T cells, Relay of herpes simplex virus between Langerhans cells and dermal dendritic cells in human skin, Defective cross‐presentation of viral antigens in GILT‐free mice, Cross‐presentation of viral and self antigens by skin‐derived CD103+ dendritic cells, Impact of varicella‐zoster virus on dendritic cell subsets in human skin during natural infection, Histopathologic features of cutaneous herpes virus infections (herpes simplex, herpes varicella/zoster): a broad spectrum of presentations with common pseudolymphomatous aspects, Human papillomavirus can escape immune recognition through Langerhans cell phosphoinositide 3‐kinase activation, Depletion of Langerhans cells in human papillomavirus type 16‐infected skin is associated with E6‐mediated down regulation of E‐cadherin, Epigenetic repression of E‐cadherin by human papillomavirus 16 E7 protein, Transcriptional repression of E‐cadherin by human papillomavirus type 16 E6, An enhanced heterologous virus‐like particle for human papillomavirus type 16 tumour immunotherapy, Langerhans cells as primary target cells for HIV infection, Langerin is a natural barrier to HIV‐1 transmission by Langerhans cells, HIV‐1 transmission in the male genital tract, HIV‐1 efficient entry in inner foreskin is mediated by elevated CCL5/RANTES that recruits T cells and fuels conjugate formation with Langerhans cells, Immunological function of Langerhans cells in HIV infection, Skin microflora and bacterial infections of the skin, Endotoxin‐tolerant mice have mutations in Toll‐like receptor 4 (Tlr4), Peptidoglycan‐ and lipoteichoic acid‐induced cell activation is mediated by toll‐like receptor 2, Human Langerhans cells express a specific TLR profile and differentially respond to viruses and Gram‐positive bacteria, Single‐cell transcriptomics reveals that differentiation and spatial signatures shape epidermal and hair follicle heterogeneity, Loss of TLR2, TLR4, and TLR5 on Langerhans cells abolishes bacterial recognition, Langerhans cells favor skin flora tolerance through limited presentation of bacterial antigens and induction of regulatory T cells, American tegumentary leishmaniasis: a quantitative analysis of Langerhans cells presents important differences between, CD8α‐ and Langerin‐negative dendritic cells, but not Langerhans cells, act as principal antigen‐presenting cells in leishmaniasis, Langerhans cells are negative regulators of the anti‐, Comparison of Th1 and Th2 responses in non‐healing and healing patients with cutaneous leishmaniasis, Langerhans cells promote early germinal center formation in response to, C‐type lectin Langerin is a β‐glucan receptor on human Langerhans cells that recognizes opportunistic and pathogenic fungi, Langerhans cell accumulation in chronic tinea pedis and pityriasis versicolor, Human epidermal Langerhans cells induce cellular immune response to trichophytin in dermatophytosis, Th17 cells confer long‐term adaptive immunity to oral mucosal, Langerhans cells require MyD88‐dependent signals for, Immunological activation of dermal Langerhans cells in contact with lymphocytes in a model of human inflamed skin, CD1a on Langerhans cells controls inflammatory skin disease, Anti‐inflammatory role of Langerhans cells and apoptotic keratinocytes in ultraviolet‐B‐induced cutaneous inflammation, Apposition of mononuclear cells to Langerhans cells in contact allergic reactions. 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Skin cells are made in the Tumour microenvironment retention and degradation have no conflict of interest to declare Clausen.

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