Calcitonin gene-related peptide and nitric oxide are involved in ultraviolet radiation-induced immunosuppression

Gillardon, Frank; Moll, Ingrid; Michel, Sabine; Benrath, Justus; Weihe, Eberhard; Zimmermann, M.

doi:10.1016/0926-6917(95)90060-8

Cited by 69 publications

(44 citation statements)

References 22 publications

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“…Hosoi et al (16) demonstrated that LCs often lie in apposition with epidermal nerves containing CGRP. Also CGRP is required for UVB-mediated suppression of contact hypersensitivity (CH) (17,18). Other studies support the potential suppression of delayed-type hypersensitivity as well as CH by CGRP (19).…”

Section: Discussionmentioning

confidence: 76%

“…The potential therapeutic effects of UV radiation in inflammatory disorders, including atopic dermatitis and psoriasis, are also described (28). Because CGRP is required for the suppression of CH by UVB (18,19), CGRP may influence responses to phototherapy. Accordingly, selective activation of CGRP-R1 on DCs might prove useful in the treatment of inflammatory skin disorders.…”

Section: Discussionmentioning

confidence: 99%

“…The cellular mechanisms involved in regulation of CH induction by UV radiation, especially the role of LCs, have been studied (17)(18)(19)27). The potential therapeutic effects of UV radiation in inflammatory disorders, including atopic dermatitis and psoriasis, are also described (28).…”

Section: Discussionmentioning

confidence: 99%

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Calcitonin Gene-Related Peptide Decreases Expression of HLA-DR and CD86 by Human Dendritic Cells and Dampens Dendritic Cell-Driven T Cell-Proliferative Responses Via the Type I Calcitonin Gene-Related Peptide Receptor

Carucci¹,

Ignatius²,

Yang³

et al. 2000

The Journal of Immunology

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These studies were performed to establish whether functional receptors for calcitonin gene-related peptide (CGRP) are present on human dendritic cells (DCs) and to investigate potential immunomodulatory effects of CGRP on DCs other than Langerhans cells. Reverse transcriptase-PCR revealed expression of mRNA for a type 1 CGRP receptor by mature and immature blood-derived DCs. Sequence analysis confirmed the identity of the type 1 CGRP receptor (CGRP-R1). Addition of CGRP (10−7 M) to mature and immature DCs resulted in mobilization of intracellular calcium. Treatment of immature DCs with CGRP (10−7 M), before and after maturation in monocyte-conditioned medium, resulted in decreased cell surface expression of HLA-DR MHC class II and the costimulatory molecule, CD86. Treatment of immature DCs with CGRP (10−7 M) also resulted in decreased expression of CD86, but expression of HLA-DR was unchanged. When CGRP-treated mature DCs were used to stimulate allogeneic T cells, proliferative responses were dampened (∼50%), especially at low DC:T cell ratios (1:360). This effect was not observed with CGRP-treated, immature DCs. In contrast, CGRP-treated mature or immature DCs were no less efficient than untreated DCs in driving syngeneic T cell-proliferative responses to staphylococcal enterotoxin B. We conclude that mature and immature DCs express type 1 CGRP receptors and that signaling through these receptors may dampen mature DC-driven T cell proliferation most likely via down-regulation of CD86 and HLA-DR.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

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Calcitonin Gene-Related Peptide Decreases Expression of HLA-DR and CD86 by Human Dendritic Cells and Dampens Dendritic Cell-Driven T Cell-Proliferative Responses Via the Type I Calcitonin Gene-Related Peptide Receptor

Carucci¹,

Ignatius²,

Yang³

et al. 2000

The Journal of Immunology

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“…Previous studies have shown that CGRP can modulate the immune response through inhibition of antigen presentation cell activity in Langerhans cells, and this mechanism has been found to be involved in ultraviolet radiation-induced immunosuppression (Hosoi et al, 1993;Gillardon et al, 1995). CGRP is an active player in neurogenic inflammation, and it is believed that CGRP is involved in the pathophysiology of migraine and other facial pains (Richardson and Vasko, 2002).…”

Section: Introductionmentioning

confidence: 99%

Two alphaherpesvirus latency-associated gene products influence calcitonin gene-related peptide levels in rat trigeminal neurons

Hamza

Higgins

Ruyechan

2007

Neurobiology of Disease

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Herpes simplex virus type-1 (HSV-1) initially infects mucoepithelial tissues of the eye and the orofacial region. Subsequently, the virus is retrogradely transported through the axons of the trigeminal sensory neurons. HSV-1 establishes a life-long latent infection in these neurons, during which the transcription of the viral genome is silent, except for the sequences encoding the latency associated transcript (LAT). To determine if HSV-1 latency might affect calcitonin gene-related peptide (CGRP) expression in trigeminal sensory neurons, we transfected primary neuronal cultures of trigeminal ganglia from rat embryos with plasmids expressing LAT. In the presence of Bone Morphogenetic Protein-7 (BMP7), CGRP was expressed in 49% of sensory neurons. However, this percentage was reduced to 19% in neurons transfected with LAT expressing plasmids. We also found that transfection of the IE63 gene of varicella-zoster virus (VZV) reduced the percentage of trigeminal neurons containing CGRP. However, the observed effect of IE63 in contrast to that of LAT, was completely reversed by treatment of cultures with MgCl 2 , which indicates that the effect of IE63 was due to increased release of CGRP from trigeminal neurons. We provide here the first evidence that HSV-1 LAT decreases the level of CGRP in trigeminal neurons. These effects may be important for reducing the neuroinflammatory response, thus protecting host neuronal cells during HSV-1 latency in trigeminal neurons. In contrast, increased release of CGRP in the presence of IE63 protein may contribute to the neuralgias associated with VZV infection.

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“…There is also recent evidence that UVA can affect the immune system. [29] calcitonin gene related peptide [30], α melanocyte stimulating hormone [31], and platelet activating factor [32], induce reactive oxygen species that contribute to impairment of the function of antigen presenting cells [25] and induce T-regulatory cell activity [33]. El-Ghorr and Norval compared immunosuppressve effects of NBUVB and broad-band UVB.…”

Section: Ultraviolet Radiationmentioning

confidence: 99%

Photo (Chemo) Therapy and Vitiligo

2015

J Turk Acad Dermatol

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Background: Vitiligo is an acquired idiopathic pigmentary skin disorder characterized by sharply demarcated milky white macules with variable size and shape. It has an estimated worldwide incidence of 0.5-4% and occurs in half of the patients before the age of 20 years. Since exact pathogenic mechanism is unknown, several proposed hypotheses are alternation of cellular and humoral immunity, melanocyte damage stimulated by chemicals released from nerve endings, structural aberration of melanocytes, melanocytorrhagia, epidermal cytokines, metabolic dysregulations and convergence theory depended on combination of these etiologic factors. Treatment of vitiligo depends on viable melanocyte reservoirs which induce repigmentation during various therapies. Although melanocyte reservoir mainly shown as hair follicle unit, repigmentation arise from three main sources. These are hair follicle unit, melanocytes located at the edge of vitiligo lesion and unaffected melanocytes within areas of depigmented epidermis. Treatment modalities for vitiligo therapy divided in three main groups as medical therapy, phototherapy and surgical therapy. Vitiligo lesions should be initially treated with topical medical therapy or localized phototherapy. If depigmentation is larger than 10-20% of body surface area, systemic medical therapy or phototherapy should be sought. When depigmentations do not regress in spite of appropriate interventions, surgical therapies should be considered as the lesions become refrectory and stable. In this review, we discuss the literature and evidence base for phototherapy in vitiligo and summarized previous studies.

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Calcitonin gene-related peptide and nitric oxide are involved in ultraviolet radiation-induced immunosuppression

Cited by 69 publications

References 22 publications

Calcitonin Gene-Related Peptide Decreases Expression of HLA-DR and CD86 by Human Dendritic Cells and Dampens Dendritic Cell-Driven T Cell-Proliferative Responses Via the Type I Calcitonin Gene-Related Peptide Receptor

Calcitonin Gene-Related Peptide Decreases Expression of HLA-DR and CD86 by Human Dendritic Cells and Dampens Dendritic Cell-Driven T Cell-Proliferative Responses Via the Type I Calcitonin Gene-Related Peptide Receptor

Two alphaherpesvirus latency-associated gene products influence calcitonin gene-related peptide levels in rat trigeminal neurons

Photo (Chemo) Therapy and Vitiligo

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