Dose response and time course for induction of T6− DR + human epidermal antigen-presenting cells by in vivo ultraviolet A, B, and C irradiation

Baadsgaard, Ole; Cooper, Kevin D.; Lisby, Steen; Wulf, Hans Christian; Wantzin, Gunhild Lange

doi:10.1016/s0190-9622(87)70265-5

Cited by 45 publications

(13 citation statements)

References 32 publications

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“…Kang et al [43] found IL-10 mRNA in NHK enriched from skin that had been UVB-exposed in vivo 48 or 72 h before. Coincidently, the same research group earlier demonstrated that UVB radiation induces the influx of CD1a ÿ DR CD36 CD11b macrophages into the epidermis, starting 24 h post-irradiation and comprising more than 5% of epidermal cells at 72 h [49][50][51]. Given the facts that (i) the increase and peak of the IL-10 mRNA signal correlates with the appearance of the macrophages in the epidermis, (ii) these macrophages are potent producers of IL-10, and (iii) the purity of the magnetic bead-selected NHK suspension was stated to be > 90% (not 100%), it is tempting to believe that the IL-10 mRNA detected by Kang et al [43] must be macrophage-derived.…”

Section: Discussionmentioning

confidence: 99%

In contrast to their murine counterparts, normal human keratinocytes and human epidermoid cell lines A431 and HaCaT fail to express IL-10 mRNA and protein

Teunissen¹,

Koomen²,

Jansen

et al. 1997

Clinical and Experimental Immunology

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SUMMARYIn mice, keratinocyte-derived IL-10 is up-regulated by ultraviolet-B (UVB) radiation and plays a major role in UVB-induced immunosuppression. The present study was designed to examine whether a comparable phenomenon can be detected in man. Freshly isolated or cultured normal human keratinocytes (NHK) and keratinocyte cell lines A431 and HaCaT were stimulated with graded doses of UVB (up to 200 J/m 2 ) or with a variety of other stimuli. RNA was extracted at various time points post-stimulation and analysed by reverse transcriptase-polymerase chain reaction (RT-PCR) using four different IL-10-specific primer pairs and RNA from monocytes or T cells as positive controls. We failed to detect IL-10 mRNA in NHK from 40 different donors (breast, abdomen, leg, scalp, foreskin) and in A431 and HaCaT cells, irrespective of the stimulation used and despite successful stimulation. Supernatants of NHK, A431 and HaCaT cultures were negative for IL-10 protein, as tested by four different ELISAs and a bioassay. Murine keratinocytes, stimulated under comparable conditions and tested by the same techniques, displayed a strong expression of IL-10 mRNA and protein. Remarkably, an IL-10 mRNA signal could be detected in NHK after a second round of PCR amplification. Because NHK suspensions are contaminated with Langerhans cells, melanocytes and possibly fibroblasts, we tested pure populations of each individual cell type to determine the origin of this IL-10 mRNA. Our results clearly indicate that NHK, Langerhans cells and fibroblasts fail to express IL-10 and that melanocytes are the principal source of IL-10 mRNA in normal human epidermis.

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Section: Discussionmentioning

confidence: 99%

In contrast to their murine counterparts, normal human keratinocytes and human epidermoid cell lines A431 and HaCaT fail to express IL-10 mRNA and protein

Teunissen¹,

Koomen²,

Jansen

et al. 1997

Clinical and Experimental Immunology

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“…Thus, both Tregs and Bregs may exhibit a negative regulatory function not only in allograft rejection but also suppression of psoriasis. We do know that relatively high, inflammatory doses of sunlight are required for the induction of Tregs and skin infiltrating suppressor macrophages, while exposure to lower subinflammatory doses of UV leads to Breg activation and suppression of immunity by inhibiting effector and memory T‐cell activation . To that end, Rutter et al .…”

Section: Link Between Photosensitive Psoriasis Uv Resistance and Polmentioning

confidence: 99%

Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?

Wolf

Weger

Patra

et al. 2016

Experimental Dermatology

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Psoriasis commonly responds beneficially to UV radiation from natural sunlight or artificial sources. Therapeutic mechanisms include the proapoptotic and immunomodulating effects of UV, affecting many cells and involving a variety of pro-and anti-inflammatory cytokines, downregulating the Th17/IL-23 response with simultaneous induction of regulatory immune cells. However, exposure to UV radiation in a subset of psoriasis patients leads to exacerbation of the disease. We herein shed light on the predisposing factors of photosensitive psoriasis, including genetics (such as HLACw*0602 or CARD14), gender and coexisting photodermatoses such as polymorphic light eruption (PLE) in the context of potential molecular mechanisms behind therapeutic photoresponsiveness or photoaggravation. UV-induced damage/pathogenassociated molecular patterns, damage to self-coding RNA (signalling through Toll-like receptors), certain antimicrobial peptides and/or inflammasome activation may induce innate immunity, leading to psoriasis at the site of UV exposure when there is concomitant, predisposing resistance against UV-induced suppression of the adaptive immune response (like in PLE) that otherwise would act to reduce psoriasis. K E Y W O R D S

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“…These infiltrating DC expressed the monocyte specific marker, OKM5 (CD36), 271 suggesting that these cells were of the monocyte/macrophage lineage. They had the ability to induce T‐cell proliferation and were able to act as stimulators of an autologous mixed epidermal cell lymphocyte reaction, 271 and were subsequently shown to express MHC II 17 …”

Section: Ultraviolet‐induced Macrophagesmentioning

confidence: 99%

Ultraviolet light induced injury: Immunological and inflammatory effects

2001

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Summary This article reviews many of the complex events that occur after cutaneous ultraviolet (UV) exposure. The inflammatory changes of acute exposure of the skin include erythema (sunburn), the production of inflammatory mediators, alteration of vascular responses and an inflammatory cell infiltrate. Damage to proteins and DNA accumulates within skin cells and characteristic morphological changes occur in keratinocytes and other skin cells. When a cell becomes damaged irreparably by UV exposure, cell death follows via apoptotic mechanisms. Alterations in cutaneous and systemic immunity occur as a result of the UV-induced inflammation and damage, including changes in the production of cytokines by keratinocytes and other skin-associated cells, alteration of adhesion molecule expression and the loss of APC function within the skin. These changes lead to the generation of suppressor T cells, the induction of antigen-specific immunosuppression and a lowering of cell-mediated immunity. These events impair the immune system's capacity to reject highly antigenic skin cancers. This review gives an overview of the acute inflammatory and immunological events associated with cutaneous UV exposure, which are important to consider before dealing with the complex interactions that occur with chronic UV exposure, leading to photocarcinogenesis.

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Dose response and time course for induction of T6− DR + human epidermal antigen-presenting cells by in vivo ultraviolet A, B, and C irradiation

Cited by 45 publications

References 32 publications

In contrast to their murine counterparts, normal human keratinocytes and human epidermoid cell lines A431 and HaCaT fail to express IL-10 mRNA and protein

In contrast to their murine counterparts, normal human keratinocytes and human epidermoid cell lines A431 and HaCaT fail to express IL-10 mRNA and protein

Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?

Ultraviolet light induced injury: Immunological and inflammatory effects

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