Nociceptive Sensory Fibers Drive Interleukin-23 Production from CD301b+ Dermal Dendritic Cells and Drive Protective Cutaneous Immunity

Kashem, Sakeen W.; Riedl, Maureen; Chen, Yao; Honda, Christopher N.; Vulchanova, Lucy; Kaplan, Daniel H.

doi:10.1016/j.immuni.2015.08.016

Cited by 321 publications

(287 citation statements)

References 80 publications

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“…Conversely, filamentous forms induced Th1 responses due to the absence of dectin-1 ligation [119]. Furthermore, the Kaplan group has shown that nociceptive sensory fibers drive IL-23 production in dermal DC, leading to the induction of IL-17 by dermal γδ T cells and subsequent activation of neutrophil antimicrobial activity, and conferring protection against C. albicans cutaneous infections [120]. …”

Section: Dendritic Cellsmentioning

confidence: 99%

Antifungal Innate Immunity: A Perspective from the Last 10 Years

Salazar¹,

Brown²

2018

J Innate Immun

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Fungal pathogens can rarely cause diseases in immunocompetent individuals. However, commensal and normally nonpathogenic environmental fungi can cause life-threatening infections in immunocompromised individuals. Over the last few decades, there has been a huge increase in the incidence of invasive opportunistic fungal infections along with a worrying increase in antifungal drug resistance. As a consequence, research focused on understanding the molecular and cellular basis of antifungal immunity has expanded tremendously in the last few years. This review will provide an overview of the most exciting recent advances in innate antifungal immunity, discoveries that are helping to pave the way for the development of new strategies that are desperately needed to combat these devastating diseases.

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Section: Dendritic Cellsmentioning

confidence: 99%

Antifungal Innate Immunity: A Perspective from the Last 10 Years

Salazar¹,

Brown²

2018

J Innate Immun

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“…There is evidence that nerve-derived CGRP induces that IL-23 release. Kashem et al [66] describe a similar pathway in which Candida albicans acts as a stimulus for CGRP release from sensory neurons, which in turn binds receptors on CD301b+ dermal dendritic cells causing release of IL-23 that then induces γδT cells to produce IL-17. This study investigated the critical role of CGRP in C. albicans immunity, as IL-17 is required for resistance to this pathogen [67, 68].…”

Section: Calcitonin Gene-related Peptidementioning

confidence: 99%

“…This study investigated the critical role of CGRP in C. albicans immunity, as IL-17 is required for resistance to this pathogen [67, 68]. They also found that ablation of sensory neurons increased susceptibility to C. albicans infection and was reversed by exogenous addition of CGRP [66]. …”

Section: Calcitonin Gene-related Peptidementioning

confidence: 99%

Immunoregulatory Effects of Neuropeptides on Endothelial Cells: Relevance to Dermatological Disorders

Mehta

Granstein²

2019

Dermatology

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Many skin diseases, including psoriasis and atopic dermatitis, have a neurogenic component. In this regard, bidirectional interactions between components of the nervous system and multiple target cells in the skin and elsewhere have been receiving increasing attention. Neuropeptides released by sensory nerves that innervate the skin can directly modulate functions of keratinocytes, Langerhans cells, dermal dendritic cells, mast cells, dermal microvascular endothelial cells and infiltrating immune cells. As a result, neuropeptides and neuropeptide receptors participate in a complex, interdependent network of mediators that modulate the skin immune system, skin inflammation, and wound healing. In this review, we will focus on recent studies demonstrating the roles of α-melanocyte-stimulating hormone, calcitonin gene-related peptide, substance P, somatostatin, vasoactive intestinal peptide, pituitary adenylate cyclase-activating peptide, and nerve growth factor in modulating inflammation and immunity in the skin through their effects on dermal microvascular endothelial cells.

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“…Interestingly, about 30% of psoriatic patients with traumatic spinal cord injury or surgical denervation developed local skin and nail fungal infections visible on the site below the neurological level of damage [103,105]. Since psoriasis is an IL-17-mediated disease and IL-17 immunity is required for antifungal immunity [12,106], the above clinical observations suggest that protection against fungal infections could also depend on neurogenic immunomodulation, as indirectly shown by animal studies demonstrating the function played by nociceptive sensory fibres in co-ordinating IL-17-dependent resistance to C. albicans infections [107]. Further evidence supporting the role played by neurogenic immunomodulation in human psoriasis and atopic dermatitis has been documented in histological studies describing an increased skin innervation in patients in comparison to healthy subjects, as well as an increased expression of sensory neuropeptides and their receptors on immune cells [108,109].…”

Section: Neurogenic T Cell Immunomodulationmentioning

confidence: 99%

Modulation of CD4+ T Helper Cell Memory Responses in the Human Skin

Padovan

2017

Int Arch Allergy Immunol

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Immunological memory is defined as the capacity to mount faster and more effective immune responses against antigenic challenges that have been previously encountered by the host. CD4+ T helper (Th) cells play central roles in the establishment of immunological memory as they assist the functions of other leukocytes. Th cells express polarized cytokine profiles and distinct migratory and seeding capacities, but also retain a certain functional plasticity that allows them to modulate their proliferation, activity, and homing behaviour upon need. Thus, in healthy individuals, T cell immunomodulation fulfils the task of eliciting protective immune responses where they are needed. At times, however, Th plasticity can lead to collateral tissue damage and progression to autoimmune diseases or, conversely, incapacity to reject malignant tissues and clear chronic infections. Furthermore, common immune players and molecular pathways of diseases can lead to different outcomes in different individuals. A mechanistic understanding of those pathways is therefore crucial for developing precise and curative medical interventions. Here, I focus on the skin microenvironment and comprehensively describe some of the cellular and molecular determinants of CD4+ T cell memory responses in homeostatic and pathological conditions. In discussing the cellular network orchestrating cutaneous immunity, I comprehensively describe the bidirectional interaction of skin antigen-presenting cells and mononuclear phagocytes with Th17 lymphocytes, and examine how the outcome of this interaction is influenced by endogenous skin molecules, including sodium salts and neuropeptides.

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Nociceptive Sensory Fibers Drive Interleukin-23 Production from CD301b+ Dermal Dendritic Cells and Drive Protective Cutaneous Immunity

Cited by 321 publications

References 80 publications

Antifungal Innate Immunity: A Perspective from the Last 10 Years

Antifungal Innate Immunity: A Perspective from the Last 10 Years

Immunoregulatory Effects of Neuropeptides on Endothelial Cells: Relevance to Dermatological Disorders

Modulation of CD4+ T Helper Cell Memory Responses in the Human Skin

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