Phytophotodermatitis Research Articles

Elimination of ketoprofen from the stratum corneum after topical administration with ketoprofen formulations in human subjects

To assess the drug concentrations and elimination rate of ketoprofen in the stratum corneum following topical administration of two different formulations in human subjects for reference in the risk management of photocontact dermatitis caused by topical ketoprofen. Ketoprofen tape and gel were used as test formulations. The stratum corneum at the application sites was removed by tape-stripping at scheduled times after removal of the formulations. The ketoprofen concentration in the stratum corneum was determined by liquid chromatography with tandem mass spectrometry. The ketoprofen concentration in the stratum corneum decreased and the elimination half-life in the stratum corneum was comparable between tape and gel after removal of the test formulations. The ketoprofen concentration in the stratum corneum decreased more rapidly after the subjects took a shower. Ketoprofen was not detected in the stratum corneum adjacent to the tape application sites. Ketoprofen in the stratum corneum appears to reach the lower limit of quantitation (0.005 μg) 12-16 days after removal of tape or gel. This period is similar to that recommended for avoiding ultraviolet light after removal of topical ketoprofen formulations in the Summary of Product Characteristics for topical ketoprofen in the European Union.

Benzophenone-3: A Potential Cause in Individuals with Undiagnosed Dermatitis

Benzophenone-3 (BP-3) is a compound that is incorporated into cosmetics and other personal hygiene products for its sunscreening effects. BP-3 is a known cause of photocontact and allergic contact dermatitis. In this study, 231 personal care products (114 from the United States and 117 from China) were examined to determine how often BP-3 was present and in what concentrations. The products fell into seven categories: …

Benzophenones

Benzophenones are ultraviolet light filters that have been documented to cause a myriad of adverse cutaneous reactions, including contact and photocontact dermatitis, contact and photocontact urticaria, and anaphylaxis. In recent years, they have become particularly well known for their ability to induce allergy and photoallergy. Topical sunscreens and other cosmetics are the sources of these allergens in most patients, but reports of reactions secondary to use of industrial products also exist. Benzophenones as a group have been named the American Contact Dermatitis Society's Allergen of the Year for 2014 to raise awareness of both allergy and photoallergy to these ubiquitous agents.

The ultrastructural effects of long-term use of henna on the albino rat skin.

Tattooing with henna is a routine practice in the Arab world. To the best of our knowledge, no previous studies have evaluated the adverse histological effects following henna tattooing on the ultrastructure of the skin. The objectives of this study were to diagnose the cytopathological alterations induced by commercial henna and to investigate the adverse role of henna when combined with sun ray on the skin. The skin of albino rats was tattooed with natural and black henna for three months, skin samples were examined by transmission electron microscope. In addition, the concentration of lead in henna samples was estimated by using atomic absorption spectrophotometry. The results expanded the understanding of the pathogenesis of henna-induced phytophotodermatitis. We hypothesized that henna-associated additives penetrated the epidermal barrier to gain access to the vascular dermis where the harmful ingredients became concentrated, leading to skin pathology through a dual mechanism. First, these ingredients became re-transported into the epidermis through vesicular trafficking leading to dermo-epidermal blistering and cytoplasmic vacuolization of the stratum basal cells. Following this, cytoplasmic vacuoles poured their content into the nuclei through continuities with the perinuclear cisterna, possibly leading to genetic mutation. The progression of keratinocytes into the next layers became associated with nuclear and cytoplasmic signs of apoptosis with subsequent phagocytosis in other epidermal cells, most probably keratinocytes. The second mechanism of injury was mediated through accumulation of inflammatory cells around capillaries in the dermis with the release of angiogenic and mitogenic mediators resulting in vasculopathy.

Normal minimal erythema dose responses in patients with suspected photosensitivity disorders

Our study identified the most common diagnoses in patients with a history of photosensitivity or with a photodistributed eruption and normal minimal erythema dose (MED) responses. We retrospectively reviewed the diagnoses and phototest results of 319 patients who were phototested at the New York University Photomedicine Section of the Charles C. Harris Skin and Cancer Pavilion from 1993 to 2009. Patients were phototested if they had a history of photosensitivity or had an eruption with a distribution that suggested photosensitivity. The majority of patients with normal MEDs were diagnosed with polymorphous light eruption, followed by contact or photocontact dermatitis, photodistributed dermatitis not otherwise specified (idiopathic), solar urticaria and photoexacerbated atopic dermatitis. The clinical history of photosensitivity and physical findings remain as important metrics in the diagnosis of patients with photodistributed dermatoses and normal MEDs.

Contact Dermatitis and Related Disorders

Contact dermatitis is an acute or chronic skin inflammation resulting from interaction with a chemical, biologic, or physical agent. This chapter discusses the major types of contact dermatitis, including irritant contact dermatitis and allergic contact dermatitis (ACD), and their predisposing factors, pathogenesis, diagnosis, risk reduction, and treatment. Also reviewed are specific etiologic forms of contact dermatitis (including topical medication allergy dermatitis, systemic contact dermatitis, clothing, textile and shoe dermatitis, and occupational contact dermatitis) as well as subtypes of contact dermatitis (including photosensitivity and latex allergy dermatitis). Figures show different types of dermatitis (such as chronic eczematous dermatitis, acute and ACD, and photocontact dermatitis), along with specific reactions from causes such as wearing a bib, a leather hatband, or sandals and from poison oak, glyceryl thioglycolate, tosylamide formaldehyde resin, rosin applied to a violin bow, bacitracin, and powdered natural rubber latex gloves. Tables list body sites affected by contact allergens, misconceptions about ACD, criteria for determining who should be given a patch test, key points in diagnosis of ACD, North America patch-test results from 2003 through 2004, topical sensitizers and potential systemic cross-reactants, substances that may cause systemic contact dermatitis, clinical features of systemic contact dermatitis, criteria for establishing occupational causation of contact dermatitis, topical and systemic photosensitizers, and distinguishing features of phototoxic versus photoallergic contact dermatitis. A sidebar lists Internet resources on contact dermatitis. This review contains 12 highly rendered figures, 11 tables, and 160 references.

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

Topical application of ketoprofen (KP) clinically evokes the allergic type of photocontact dermatitis. To avoid this adverse reaction, we investigated the beneficial effect of each ultraviolet (UV) filter that was included in topical ketoprofen formulation. We first tested the inhibitory effects of four UVA filters by a modified local lymph node assay following KP application on the mouse skin and UVA irradiation on the same site. In this assessment, butyl methoxy dibenzoylmethane (BMDBM), when included in KP application, exerted the most effective inhibitory effect on stimulation with KP and UVA. We manufactured topical patch and gel KP applicants containing BMDBM, which retained KP penetration through the skin and KP stability toward UVA. The ability of BMDBM in these formulations to inhibit KP photosensitivity was evaluated by a modified adjuvant and strip method in guinea pigs, and the photoallergic reactions induced by the BMDBM-containing KP applicants were lower than the non-containing ones. It is known that KP has a cross-reactivity with benzophenone upon UVA exposure, but such a photocross-reactivity of BMDBM with KP was not observed in a mouse ear swelling model. The anti-inflammatory effect of the BMDBM-containing KP patch applicant was comparable to the non-containing one. These results suggest that the addition of BMDBM into KP topical formulations is efficacious for inhibition of KP photocontact dermatitis.

Photoallergy

Photoallergy is an entity of allergy in the dermatological field. Sunlight is involved in the pathophysiology of photoallergy. Photoallergy is classified into intrinsic and extrinsic diseases. As extrinsic diseases, photosensitivity due to drugs and photocontact dermatitis are important for physicians as well as dermatologists. Physicians should have accurate understanding of these disorders.

Photoallergic contact dermatitis to 8‐methoxypsoralen in Ficus carica

Photocontact dermatitis to Ficus carica is induced by furocoumarins present in sap. These substances are generally considered to cause phototoxic reactions. We conducted a patch test and histopathological study of patients with phytophoto contact dermatitis from the fig tree to evaluate the mechanism underlying the photoreaction. Patch and photopatch testing with serial dilutions of two natural furocoumarins [5-methoxypsoralen and 8-methoxypsoralen (8-MOP)] contained in plant sap were performed in 47 patients. A synthetic furocoumarin, 4,5',8-trimethylpsoralen, was also tested. Histopathological analyses were made of some positive photoreactions. Positive photopatch tests reactions to 8-MOP were obtained in 12 of 47 patients, in 4 of them down to a concentration of 0.0001%. Patch tests and photopatch tests to the other two furocoumarins were negative. Histopathological findings on biopsies from positive photopatch tests to 8-MOP showed a dermatitis. Allergic photoreactions induced by contact with plants containing coumarins are generally regarded as chance findings. This study has demonstrated that phytophoto allergic contact dermatitis resulting from furocoumarins is not an exceptional finding, and should be suspected in subjects with diffuse clinical manifestations in photo-exposed but also non-exposed sites. To differentiate allergic from toxic photoreactions, patch tests need to be performed with serial dilutions of furocoumarins. Histological analysis of a biopsy sample from a positive test site will reveal alterations compatible with a photoallergic contact dermatitis.

Epidemiología de la dermatitis de contacto: prevalencia de sensibilización a diferentes alérgenos y factores asociados

Background In clinical practice, contact dermatitis is a relatively common skin complaint, whose prevalence has increased in recent years. Study by patch testing is essential for diagnosis of contact sensitization. Objectives To study the prevalence of sensitization to different allergens in a standard battery and observe the influence of different epidemiological and clinical variables on contact sensitization. A large number of allergens were included in our battery in order to detect new sensitizations whose prevalence might justify further study. Material and methods This was a retrospective, observational, epidemiological study of 1092 patients, conducted in our skin allergy unit between January 1, 2000, and December 31, 2005. All patients were studied with a battery of 51 allergens. We assessed the following variables: sex, age, type of referral, occupation, site and course of skin lesions, personal and family history of atopy, positive patch tests, clinical significance, diagnosis, source of sensitization, and occupational relationship. Results At least 1 positive result was found in 55% of the patients, and 55.7% presented atopic dermatitis in one of its clinical variants: allergic contact dermatitis (28.2%), irritant contact dermatitis (20.1%), photoallergic contact dermatitis (2.2%), and phototoxic contact dermatitis (1.2%). The most prevalent allergens were nickel sulfate (29.3%), palladium chloride (11.7%), cobalt chloride (10.8%), potassium dichromate (7.5%), fragrance blends (6.3%), and p-phenylenediamine (6.1%). A positive occupational relationship was found in 41.1%, and 21.3% of the patients studied were diagnosed with occupational contact dermatitis. Metalworkers, construction workers, and professional hairdressers were the most strongly represented groups. The most common source of sensitization was contact with metallic objects, followed by drugs, cosmetics, and rubber items. Female sex was the only independent variable that had a significant influence on the risk of contact sensitization in general. Conclusion Women became sensitized at a younger age than men, and the frequency of positive results in the patch tests increased with age, reaching a maximum at between 60 and 69 years of age, when the greatest rate of sensitization occurred. Comparison of our results with other Spanish data showed a progressive and constant increase in sensitization to nickel sulfate, fragrance blends, balsam of Peru, and rosin, and a decrease in sensitization to potassium dichromate. The inclusion of new allergens such as palladium chloride, diallyl disulfide, and p-toluene sulfonamide formaldehyde improved the sensitivity of the standard battery in the detection of contact sensitization. We therefore recommend further studies of these allergens.

Epidemiology of Contact Dermatitis: Prevalence of Sensitization to Different Allergens and Associated Factors

Background In clinical practice, contact dermatitis is a relatively common skin complaint, whose prevalence has increased in recent years. Study by patch testing is essential for diagnosis of contact sensitization. Objectives To study the prevalence of sensitization to different allergens in a standard battery and observe the influence of different epidemiological and clinical variables on contact sensitization. A large number of allergens were included in our battery in order to detect new sensitizations whose prevalence might justify further study. Material and methods This was a retrospective, observational, epidemiological study of 1092 patients, conducted in our skin allergy unit between January 1, 2000 and December 31, 2005. All patients were studied with a battery of 51 allergens. We assessed the following variables: sex, age, type of referral, occupation, site and course of skin lesions, personal and family history of atopy, positive patch tests, clinical significance, diagnosis, source of sensitization, and occupational relationship. Results At least 1 positive result was found in 55% of the patients, and 55.7% presented contact dermatitis in one of its clinical variants: allergic contact dermatitis (28.2%), irritant contact dermatitis (20.1%), photoallergic contact dermatitis (2.2%), and phototoxic contact dermatitis (1.2%). The most prevalent allergens were nickel sulfate (29.3%), palladium chloride (11.7%), cobalt chloride (10.8%), potassium dichromate (7.5%), fragrance blends (6.3%), and p-phenylenediamine (6.1%). A positive occupational relationship was found in 41.1%, and 21.3% of the patients studied were diagnosed with occupational contact dermatitis. Metalworkers, construction workers, and professional hairdressers were the most strongly represented groups. The most common source of sensitization was contact with metallic objects, followed by drugs, cosmetics, and rubber items. Female sex was the only independent variable that had a significant influence on the risk of contact sensitization in general. Conclusion Women became sensitized at a younger age than men, and the frequency of positive results in the patch tests increased with age, reaching a maximum at between 60 and 69 years of age, when the greatest rate of sensitization occurred. Comparison of our results with other Spanish data showed a progressive and constant increase in sensitization to nickel sulfate, fragrance blends, balsam of Peru, and Colophonium, and a decrease in sensitization to potassium dichromate. The inclusion of new allergens such as palladium chloride, diallyl disulfide, and p-toluene sulfonamide formaldehyde improved the sensitivity of the standard battery in the detection of contact sensitization. We therefore recommend further studies of these allergens.

Photoallergy

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.

Chronic Actinic Dermatitis: Clinical Cases, Diagnostic Workup, and Therapeutic Management

We report four cases of chronic actinic dermatitis (CAD) occurring in middle-aged men with significant outdoor exposure. The aim of this report is to show the spectrum of presentations of patients with CAD and to outline the proper diagnostic workup of these individuals. Phototesting was performed to determine the minimal erythema doses to ultraviolet (UV)A (315-400 nm) and UVB (280-315 nm) and photopatch testing and patch testing for each individual with the North American Contact Dermatitis Group Standard series and the Chemotechnique Plant series, supplemented by the Hausen Plant series and the patients' own products. All patients were men, over 45 years, who worked outdoors or had outdoor hobbies. Two had a past known history of allergic contact dermatitis. Two had atopic dermatitis. Three had positive reactions to Compositae plants and sesquiterpene lactone; one had a reaction to lichen acid mix. All had photocontact dermatitis or contact dermatitis to sunscreen chemicals, including benzophenone 3 (oxybenzone), butyl methoxydibenzoylmethane (avobenzone), and ethylhexyl methoxycinnamate (octinoxate). All reacted to fragrance mix; two reacted to balsam of Peru and two to colophony. All had biopsies showing an eczematous pattern. CAD is persistent, with a classic presentation, and requires a specific diagnostic workup. Effective therapeutic options exist for patients with CAD.

Photoallergic contact dermatitis caused by ultraviolet filters in different sunscreens

Over the last decade, a change in the public awareness regarding the possible danger of excessive sunlight exposure has resulted in an increased consumption of sunscreens. These products contain a broad spectrum of putative sensitizers that can cause contact dermatitis and, upon exposure to ultraviolet (UV) irradiation, photocontact dermatitis. Among these sensitizing compounds, UV filters are the most frequent cause of photoallergic reactions. Although rarely observed, we here describe the occurrence of a photoallergic contact dermatitis in a 55-year-old man after the use of two different sunscreens. Photopatch testing showed hypersensitivity reactions of the delayed type against three different chemical UV filters, 4-tert-butyl-4- methoxy-dibenzoylmethane (Parsol 1789), 2-ethylhexyl-p-methoxycinnamate (Parsol MCX), and isoamyl-p-methoxycinnamate (Neoheliopan).

Combined photocontact dermatitis to benzydamine hydrochloride and the emulsifiers, Span 60 and Tween 60 contained in Tantum® cream

Contact DermatitisVolume 57, Issue 1 p. 61-62 Combined photocontact dermatitis to benzydamine hydrochloride and the emulsifiers, Span 60 and Tween 60 contained in Tantum® cream Ana Giménez-Arnau, Corresponding Author Ana Giménez-Arnau Department of DermatologyAna Giménez-ArnauDepartment of DermatologyHospital del MarPasseig Maritim 25-2908003 BarcelonaSpainTel: 34932099936Fax: 34934144909e-mail: 22505aga@comb.esSearch for more papers by this authorMontserrat Gilaberte, Montserrat Gilaberte Department of DermatologySearch for more papers by this authorDavid Conde, David Conde Department of Pharmacy, Hospital del Mar, IMAS, Universitat Autònoma de Barcelona, Barcelona, SpainSearch for more papers by this authorMerce Espona, Merce Espona Department of Pharmacy, Hospital del Mar, IMAS, Universitat Autònoma de Barcelona, Barcelona, SpainSearch for more papers by this authorRamon M. Pujol, Ramon M. Pujol Department of DermatologySearch for more papers by this author Ana Giménez-Arnau, Corresponding Author Ana Giménez-Arnau Department of DermatologyAna Giménez-ArnauDepartment of DermatologyHospital del MarPasseig Maritim 25-2908003 BarcelonaSpainTel: 34932099936Fax: 34934144909e-mail: 22505aga@comb.esSearch for more papers by this authorMontserrat Gilaberte, Montserrat Gilaberte Department of DermatologySearch for more papers by this authorDavid Conde, David Conde Department of Pharmacy, Hospital del Mar, IMAS, Universitat Autònoma de Barcelona, Barcelona, SpainSearch for more papers by this authorMerce Espona, Merce Espona Department of Pharmacy, Hospital del Mar, IMAS, Universitat Autònoma de Barcelona, Barcelona, SpainSearch for more papers by this authorRamon M. Pujol, Ramon M. Pujol Department of DermatologySearch for more papers by this author First published: 15 June 2007 https://doi.org/10.1111/j.1600-0536.2007.01080.xCitations: 6Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume57, Issue1July 2007Pages 61-62 RelatedInformation

Phytophotodermatitis Following PUVA and the Use of a Citrus Containing Lotion

Phytophotodermatitis Following PUVA and the Use of a Citrus Containing Lotion

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

Ketoprofen (KP) clinically evokes the allergic type of photocontact dermatitis when applied to the skin and irradiated with ultraviolet A (UVA). We have established a murine model of photocontact dermatitis to KP, which is a T cell-mediated delayed type hypersensitivity. To further explore the mechanism underlying this sensitivity, we investigated whether KP plus UVA activates the antigen-presenting ability of Langerhans cells (LCs). We analyzed the expression of surface molecules on LCs in the murine epidermis treated with KP plus UVA by immunohistochemistry and flow cytometry. Changes in the cytokine expression of epidermal cells from KP-phototreated skin were also examined by real-time PCR. LCs became larger after treatment with KP plus UVA. The number of LCs was significantly decreased 2-3 days after KP phototreatment and recovered on day 5. A flow cytometric analysis revealed that KP plus UVA increased the percentage of LCs that highly expressed MHC class II, CD86, CD80, CD54 and CD40, whereas neither KP nor UVA alone enhanced the expression. KP phototreatment augmented the expression of I-A and CD86 on LCs in KP and UVA dose-dependent manners. A real-time PCR analysis of KP-phototreated skin showed that the expression of mRNA for IL-1alpha and GM-CSF was immediately increased after treatment. A photosensitizing regimen of KP plus UVA activates LCs at least partly by stimulating keratinocytes to produce cytokines. Two strains of mice (BALB/c and AKR) differ in responsiveness to KP and the difference is not related to the activation of keratinocytes.

Induction of keratinocyte apoptosis by photosensitizing chemicals plus UVA

The capacity of photosensitizing chemicals with ultraviolet A light (UVA) to induce apoptosis is one of the methods to assess their phototoxic and potentially photoallergic properties, since apoptotic cells may be easily presented by antigen-presenting cells. We examined the photoaggravated ability to induce keratinocyte apoptosis of various chemicals that are known as causative agents of photocontact dermatitis and drug photosensitivity involving photoallergic and/or phototoxic mechanisms. HaCaT keratinocytes were incubated with 3,3',4',5-tetrachlorosalicylanilide (TCSA), bithionol, diphenylhydramine, chlorpromazine, 6-methylcoumarin, sparfloxacin, and enoxacin at 10(-7) to 10(-4)M and irradiated with UVA at 4J/cm(2). As positive control, 8-methoxypsoralen (8-MOP) was also tested. Apoptosis and necrosis were evaluated by flow cytometric enumeration of annexin V(+) 7-AAD(-) and annexin V(+) 7-AAD(+) cells, respectively. The expression of apoptosis-related molecules, caspase-3 and poly (ADP-ribose) polymerase (PARP), was tested by flow cytometric and Western blotting analyses. In a comparison with non-irradiated cells, significant apoptosis was found in TCSA, bithionol, chlorpromazine, sparfloxacin and enoxacin at 10(-4) or 10(-5)M as well as 8-MOP as assessed by both annexin V and active caspase-3 stainings, while necrosis occurred in most of these chemicals at 10(-4)M. Neither apoptosis nor necrosis was seen in diphenylhydramine or 6-methylcoumarin. PARP were activated in HaCaT cells phototreated with TCSA, bithionol and chlorpromazine. We suggest that our method is useful for in vitro assessment of phototoxicity and potential photoallergenicity of chemicals.

Fotodermatitis de contacto por dexketoprofeno. Descripción de dos casos

Dexketoprofen is the active isomer of ketoprofen and likewise belongs to the group of non-steoidal anti-inflammatory drugs (NSAIDs) derived from propionic acid. We have recently studied, using patch and photopatch tests, two women with a characteristic clinical picture of contact photo-dermatitis who had used topical dexketoprofen (Enangel ®) in the days before onset of the rash. In both cases we used the standard series of GEIDC, a series for NSAIDs, the product itself (Enangel ®) and its excipients. On examination of the photopatches of both patients at 96 hours we found positive reactions to dexketoprofen and Enangel ®. Furthermore, in one of the women we observed simultaneous photosensitivity to other NSAIDs and to several excipients of Enangel ®. Reviewing the literature we have found only three references on contact photodermatitis due to dexketoprofen. We describe two new cases, with multiple photosensitivities in one of them. We consider that such patients should be patch tested with dexketoprofen at 0.1-1 % petrolatum, concentrations that are notably inferior to those used in previous publications.

Establishment of murine model of allergic photocontact dermatitis to ketoprofen and characterization of pathogenic T cells

Ketoprofen is well known to evoke the allergic type of photocontact dermatitis when it is applied to the skin and irradiated with ultraviolet A (UVA) light. We aimed to establish a murine model of this photosensitivity and to characterize pathogenic T cells concerned with the sensitivity. Various strains of mice were sensitized on two consecutive days by application of ketoprofen to the shaved abdomen and irradiation of the skin with UVA. Five days later, they were elicited with ketoprofen plus UVA on the earlobes. Immune lymph node cells and epidermal cells from the challenged sites were analyzed by RT-PCR. Mice were successfully sensitized and challenged with 4% and 2% ketoprofen, respective, plus UVA at 20J/cm2. The responses in H-2k mice were higher than those in the other strains examined. Immune lymph node CD4+ or CD8+ cells from ketoprofen-photosensitized H-2k mice were transferred i.v. to naïve syngeneic recipients. Mice receiving CD4+ but not CD8+ cells exhibited ketoprofen photosensitivity, but transference of both CD4+ and CD8+ cell populations was more effective. Lymph node cells from photosensitized mice expressed high levels of mRNA for Th2 cytokine (IL-4) and Th2 chemokine receptor (CCR4) as well as Th1 cytokine (IFN-gamma) and Th1 chemokine receptor (CXCR3), as assessed by RT-PCR. In addition, epidermal cells from challenged earlobes expressed increased levels of both Th1 (TARC) and Th2 (Mig) chemokines. It is considered that not only Th1 but also Th2 cells participate in the pathogenesis of murine photocontact dermatitis to ketoprofen.