Stimulation of Langerhans cells with ketoprofen plus UVA in murine photocontact dermatitis to ketoprofen

Atarashi, Kenji; Kabashima, Kenji; Akiyama, Katsuhiko; Tokura, Y.

doi:10.1016/j.jdermsci.2007.04.001

Cited by 24 publications

(35 citation statements)

References 35 publications

(74 reference statements)

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“…The damage reactions to cells cause not only phototoxicity but also photoallergy where immune cells in the skin, such as dendritic cells and keratinocytes, are involved. KP phototreatment upregulates the antigen presenting ability of dendritic cells and promotes the production of cytokines in the epidermis [11]. The photoallergic sensitivity is divided into the photosensitization and the photoelicitation phases.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous studies have shown that KP application plus UVA irradiation induces and elicits photocontact dermatitis in mice, and both CD4 + and CD8 + T cells are required for the full-blown sensitivity reaction [10]. In addition, KP plus UVA upregulates the expression of MHC class II and costimulatory molecules on murine dendritic cells, promoting antigen-presenting ability of the cells [11]. Dendritic cells bearing KP-photoantigen sensitize photoantigen-specific T cells in draining lymph node cells [10].…”

Section: Introductionmentioning

confidence: 99%

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Addition of UVA-absorber butyl methoxy dibenzoylmethane to topical ketoprofen formulation reduces ketoprofen-photoallergic reaction

Atarashi¹,

Takano²,

Kato³

et al. 2012

Journal of Photochemistry and Photobiology B: Biology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Addition of UVA-absorber butyl methoxy dibenzoylmethane to topical ketoprofen formulation reduces ketoprofen-photoallergic reaction

Atarashi¹,

Takano²,

Kato³

et al. 2012

Journal of Photochemistry and Photobiology B: Biology

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“…Ear swelling responses are measured 24 h after challenge. In addition to TCSA, the photoallergenic potential of other halogenated salicylanilides, such as tribromosalicylanilide and bithionol [33], and ketoprofen [34,35] is also detected by this mode of sensitization.…”

Section: Mouse Model Of Photoallergic Contact Dermatitismentioning

confidence: 99%

“…Mice with H-2 b,d alleles are high responders, whereas the H-2 k haplotype is closely associated with low responders [5]. On the other hand, in photoallergic contact dermatitis to ketoprofen, H-2 k is associated with high responders and H-2 b,d with low responders [35]. Therefore, high responder H-2 haplotypes are different among photosensitivities to each photohaptenic chemical.…”

Section: Mouse Model Of Photoallergic Contact Dermatitismentioning

confidence: 99%

Photoallergy

Tokura¹

2009

Expert Review of Dermatology

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There are two mechanisms underlying photosensitivity to exogenous agents: phototoxicity and photoallergy. While the phototoxic reaction is mediated mainly by free radicals, the photoallergic reaction is induced and elicited by immunological consequences. Photosensitive chemicals have a haptenic moiety, and two hypotheses have been put forward to explain the formation of photoallergens: prohaptens and photohaptens. Photohaptens need to coexist with a protein and, upon UV irradiation, a covalent bond is formed. The vast majority of clinically photoallergic chemicals are photohaptens rather than prohaptens. In a clinical photopatch test, a causative chemical is applied to the skin and UVA is irradiated to the site. This method tests the photohaptenic property. Clinically, photocontact dermatitis and drug photosensitivity are the two major disorders caused by topical and systemic exogenous photosensitizers, respectively. In photocontact dermatitis, halogenated salicylanilide and the related compounds musk ambrette, 6-methylcoumarin and benzophenone-3 (oxybenzone), were causative and, recently, topical NSAIDs have been another leading cause. In drug photosensitivity there have been many photosensitive drugs, including quinolones, piroxicam, afloqualone, griseofluvin, tegafur and tilisolol. The underlying mechanisms involve topically applied or orally administered chemicals diffusing from the skin surface or blood to the epidermis, and epidermal cells are photoderivatized with a given chemical upon UVA irradiation. Antigen-presenting dendritic cells are photomodified with the chemical upon exposure of the skin to UVA and become photohapten-bearing, T-cell stimulatory cells.

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“…Various drugs have been reported to induce photosensitivity, including quinolones [3], afloqualone (AQ) [4], piroxicum [5], non-steroidal anti-inflammatory drugs [6], and others. There are phototoxic [2] and photoallergic [3][4][5][6][7] mechanisms in drug sensitivity, and the incidence of photoallergy is higher than that of phototoxicity [3]. Two theories of photoantigen formation have been put forward to explain the photoallergic mechanisms, prohapten and photohapten [8].…”

Section: Introductionmentioning

confidence: 99%