Update of Immune Events in the Murine Contact Hypersensitivity Model: Toward the Understanding of Allergic Contact Dermatitis

Vogt-Koyanagi-Harada Disease

The skin is a complex barrier organ made of a symbiotic relationship between microbial communities and host tissue via complex signals provided by the innate and the adaptive immune systems. It is constantly exposed to various endogenous and exogenous factors which impact this balanced system potentially leading to inflammatory skin conditions comprising infections, allergies or autoimmune diseases. Unlike the gut and stool microbiome which has been studied and described for many years, investigations on the skin or scalp microbiome only started recently. Researchers in microbiology and dermatology started using modern methods such as pyrosequencing assays of bacterial 16S rRNA genes to identify and characterize the different microorganisms present on the skin, to evaluate the bacterial diversity and their relative abundance and to understand how microbial diversity may contribute to skin health and dermatological conditions. This article aims to provide an overview on the knowledge about the skin microbiota, the microbiome and their importance in dermatology.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/jdv.13965

Microbiome in healthy skin, update for dermatologists

The human skin is an integral system that acts as a physical and immunological barrier to outside pathogens, toxicants, and harmful irradiations. Environmental ultraviolet rays (UV) from the sun might potentially play a more active role in regulating several important biological responses in the context of global warming. UV rays first encounter the uppermost epidermal keratinocytes causing apoptosis. The molecular mechanisms of UV-induced apoptosis of keratinocytes include direct DNA damage (intrinsic), clustering of death receptors on the cell surface (extrinsic), and generation of ROS. When apoptotic keratinocytes are processed by adjacent immature Langerhans cells (LCs), the inappropriately activated Langerhans cells could result in immunosuppression. Furthermore, UV can deplete LCs in the epidermis and impair their migratory capacity, leading to their accumulation in the dermis. Intriguingly, receptor activator of NF-κB (RANK) activation of LCs by UV can induce the pro-survival and anti-apoptotic signals due to the upregulation of Bcl-xL, leading to the generation of regulatory T cells. Meanwhile, a physiological dosage of UV can also enhance melanocyte survival and melanogenesis. Analogous to its effect in keratinocytes, a therapeutic dosage of UV can induce cell cycle arrest, activate antioxidant and DNA repair enzymes, and induce apoptosis through translocation of the Bcl-2 family proteins in melanocytes to ensure genomic integrity and survival of melanocytes. Furthermore, UV can elicit the synthesis of vitamin D, an important molecule in calcium homeostasis of various types of skin cells contributing to DNA repair and immunomodulation. Taken together, the above-mentioned effects of UV on apoptosis and its related biological effects such as proliferation inhibition, melanin synthesis, and immunomodulations on skin residential cells have provided an integrated biochemical and molecular biological basis for phototherapy that has been widely used in the treatment of many dermatological diseases.

/pdf/molecular-mechanisms-of-uv-induced-apoptosis-and-its-effects-480ox7ziv0.pdf

Molecular mechanisms of UV-induced apoptosis and its effects on skin residential cells: The implication in UV-based phototherapy

Advances in transcutaneous vaccine delivery: do all ways lead to Rome?

The effects of NB-UVB on the hair follicle-derived neural crest stem cells differentiating into melanocyte lineage in vitro

As cutaneous pigment-producing cells, melanocytes can become targets of primary and secondary immune response as can be seen in diseases like vitiligo and Vogt-Koyanagi-Harada (VKH) syndrome. Viral infections have previously been implicated as a possible precipitating factor in the destruction of melanocytes in these disorders. During viral replication, double-stranded RNA (dsRNA) is produced as an intermediate metabolite, which induces antiviral and inflammatory responses through Toll-like receptor 3 (TLR3) in cells of innate immune system. The functional responses of melanocytes to dsRNA, however, remain unclear. Herein, we demonstrated that human melanocytes expressed TLR3 at a constitutive and inducible level. Stimulation with poly(I:C), a synthetic dsRNA analogue, triggered apoptosis of melanocytes. The apoptosis-inducing effect was shown by RNA interference to be largely dependent on TLR3, but occurred independently of NF-κB activation since treatment with specific NF-κB inhibitor Bay 11-7082 failed to prevent the process. In contrast, IFN-β neutralizing Ab blocked the apoptosis-inducing effect of dsRNA, indicating the involvement of IFN-β autocrine signalling. Furthermore, studies on the intracellular signal transduction pathways revealed that dsRNA induces the activation of p38, ERK1/2 and JNK1/2 in melanocytes. Using specific inhibitors, we demonstrated that activation of p38 and ERK1/2 controlled both IFN-β secretion and IFN-β mediated cell death. Taken together, these data suggest that viral dsRNA stimulates TLR3 in human melanocytes and triggers the cellular apoptosis through autocrine of IFN-β.

/pdf/double-stranded-rna-induces-melanocyte-death-via-activation-7inwh69sbg.pdf

Double-stranded RNA induces melanocyte death via activation of Toll-like receptor 3.

https://www.central-lab.org/download/paper22.pdf

Cultured human melanocytes express functional toll-like receptors 2-4, 7 and 9.

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The effects of NB-UVB on the hair follicle-derived neural crest stem cells differentiating into melanocyte lineage in vitro

Double-stranded RNA induces melanocyte death via activation of Toll-like receptor 3.

Cultured human melanocytes express functional toll-like receptors 2-4, 7 and 9.