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PubMedDate not supplied

Photosensitive epilepsy beyond adolescence: is freedom from photosensitivity age-dependent?

Patients with photosensitive epilepsy (PSE) are said to lose photosensitivity with age. That is, they do not suffer from photosensitive epileptic seizures after the third decade of life. This claim seems to be an over generalised statement and does not take into account all other important confounding factors that determine the duration and process of neurological illnesses. Hence, there are contradictions pertaining to age of freedom of photosensitivity in epilepsy and in epilepsy with photosensitivity. Often patients are declared free from epileptic activity; however, some of these patients are still found to have seizures a few years later. This paper assesses the freedom photosensitivity in 58 PSE patients to ascertain validity of the claim that patients lose their photosensitivity with age. Thirty-nine of the 58 patients (67%) were female whilst (33%) were male, giving a female/male ratio of 3:1. The average age of onset of photosensitivity was 7 years. Of all the cases studied forty-one (71%) had a family history of photosensitive epilepsy, while seventeen (29%) had no family history of photosensitive epilepsy. Proof of photosensitivity in all the patients was determined by persistent EEG abnormalities including occipital spike and wave discharges. Results show that photosensitivity persisted beyond adolescence; hence, there was no specific age limit of freedom from photosensitivity in patients, especially in those with family history of photosensitive epilepsy. However, those patients who were having regular antiepileptic medication and/or were taking adequate preventive measures had a temporary period of freedom from sensitivity which lasted 1-4 years. These findings suggest that freedom from photosensitivity is not age-dependent, especially in those patients with family history of photosensitive epilepsy.

Adolescent↗

PubMed1999

Characterization of photosensitivity in the Smith-Lemli-Opitz syndrome: a new congenital photosensitivity syndrome.

Photosensitivity has recently been reported as a feature of the Smith-Lemli-Opitz syndrome (SLO). The aim of this study was to establish the photobiological features of this disorder and to examine the hypothesis that the photosensitivity is caused by the high levels of 7-dehydrocholesterol found in SLO. All known cases of SLO in the U.K. were reviewed and clinical details of photosensitivity were recorded in detail. The action spectrum of the photosensitive eruption was defined by monochromator light testing. Thirteen of the 23 subjects (57%) had severe photosensitivity, and in 10 there was no photosensitivity. No correlation was identified between levels of 7-dehydrocholesterol and severity of photosensitivity, suggesting that the photosensitivity in SLO is not caused by a direct phototoxic effect mediated by 7-dehydrocholesterol. A novel pattern of photosensitivity was observed, with onset of a sunburn-like erythema on sun-exposed skin within minutes of sun exposure, which persisted in most cases for up to 24-48 h before fading. Monochromator light testing in three subjects showed an ultraviolet (UV) A-mediated photosensitivity eruption with greatest photosensitivity at 350 nm. Photosensitivity is a common and prominent feature of SLO and appears to be UVA-mediated. Elucidation of its biochemical basis may provide insight into normal cutaneous protective mechanisms against UVA-induced photodamage, and also sun sensitivity in general.

Adolescent↗

PubMed2002

Duration of skin photosensitivity and incidence of photosensitivity reactions after administration of verteporfin.

BACKGROUND: Verteporfin (Visudyne, Novartis AG) is a light-activated drug that reduces the risk of vision loss in patients with certain types of choroidal neovascularization (CNV). Because photosensitivity can occur with photosensitizers, it is important for ophthalmologists providing verteporfin therapy to understand its time course and duration, as well as the incidence of photosensitivity reactions. METHODS: Data were obtained from three sources: 1) the time course of skin photosensitivity in 17 volunteers by measuring erythema/edema over time after verteporfin, using red light exposure; 2) the duration of skin photosensitivity in 30 patients with skin cancer by exposing skin to simulated solar light and calculating the daily minimal erythematous dose; and 3) the incidences of photosensitivity reactions as recorded in three phase III trials in patients with CNV secondary to age-related macular degeneration or pathologic myopia who received the regimen of verteporfin therapy currently approved by regulatory authorities (infusion of 6 mg/m(2) body surface area). RESULTS: 1) Skin photosensitivity was high at the first timepoint of 1.5 hours after dosing and decreased rapidly thereafter; 2) the duration of skin photosensitivity was dose dependent, ranging from 2.0 to 6.7 days at 6 to 20 mg/m(2), respectively (mean of 2 days at a dose of 6 mg/m(2)); and 3) photosensitivity reactions occurred in only 2.2% of patients in the phase III trials, including two severe events, one secondary to extravasation. All treatment-related reactions in the phase III trials occurred within the first 2 days after dosing, with the exception of two mild reactions and one moderate reaction that occurred 3 days after treatment. CONCLUSIONS: Verteporfin is associated with short-lived photosensitivity and a low incidence of photosensitivity reactions in clinical trials, most of which could probably have been avoided by adherence to protocol instructions for skin protection.

Adult↗

PubMed1992

Oxicam-induced photosensitivity. Patch and photopatch testing studies with tenoxicam and piroxicam photoproducts in normal subjects and in piroxicam-droxicam photosensitive patients.

BACKGROUND: The mechanism of piroxicam-induced photosensitivity is unknown. It was first attributed to metabolites of the drug produced in vivo but further photochemical studies disclosed that piroxicam was not stable to light, forming at least two photoproducts. Photosensitivity reactions to droxicam and tenoxicam have been not reported. OBJECTIVE: The aim of this study was to determine whether piroxicam photoproducts contribute to the light reactions induced by this drug, to describe a case of droxicam-induced photosensitivity and to study the in vivo photosensitizing potential of tenoxicam. METHODS: Patch and photopatch tests with two major photoproducts of piroxicam, with different preparations of UVA-preirradiated piroxicam, and with low and high concentrations of tenoxicam were performed in normal volunteers and in piroxicam-photosensitive patients. Phototesting studies were also performed before and after the oral administration of tenoxicam in both groups of subjects. RESULTS: Positive patch test responses were obtained in piroxicam-photosensitive patients only with the preirradiated piroxicam preparations. Phototesting studies with tenoxicam were normal in both groups. CONCLUSION: Minor or intermediate piroxicam photoproducts are more likely to be responsible for the photosensitivity reactions induced by this drug.

Adult↗

PubMed1984

The influence of intermittent light stimulation on potentials evoked by single flashes in photosensitive and non-photosensitive Papio papio.

The effects of intermittent light stimulation (ILS) on visual potentials (VEPs), evoked in different cortical areas, were statistically studied in baboons either naturally photosensitive or made photosensitive by allylglycine at a subconvulsant dose, as well as in non-photosensitive animals. VEPs were induced by single flashes (paradigm a) or by flashes preceded by trains of ILS (paradigm b). In every baboon, photosensitive or not, the VEPs induced by paradigm b in the striate area show a decrease of amplitude compared to VEPs induced by paradigm a. The ERG evolves in the same way. Therefore, these effects do not depend on photosensitivity; they depend on the intensity of stimulation. In photosensitive animals the single flash in paradigm b can induce a paroxysmal VEP in the fronto-rolandic (FR) area. In parietal and peristriate areas the VEPs induced by paradigm b show new late components when compared to those induced by paradigm a. These changes are observed even if no FR paroxysmal VEP is induced; they depend on the presence of a train of ILS preceding the single flash and on the predisposition to epilepsy (both natural and due to allylglycine); in the non-photosensitive animals the VEPs recorded in the same areas do not show such differences. We consider that among afferents which could act in inducing FR paroxysmal activities some cortico-cortical visual afferents can come from non-specific cortical areas (parietal or peristriate), but would not directly originate in the striate cortex; anatomical data in this species may support such a hypothesis.

Afferent Pathways↗

PubMedDate not supplied

Preliminary assessment of the efficacy of Org 6370 in photosensitive epileptic patients: paradoxical enhancement of photosensitivity and provocation of myoclonic seizures.

Photosensitivity has proved to be a useful model to study the acute effects of experimental antiepileptic drugs (AEDs). The photosensitivity range is usually diminished or even abolished after administration of a known or experimental AED. An increase in photosensitivity, an unexpected reaction, was found in four photosensitive epileptic patients after oral ingestion of 500, 100, or 50 mg of Org 6370. Moreover, the three patients receiving doses of 100 and 500 mg reported nausea, dizziness, restlessness, and an increase in spontaneous epileptic seizures (myoclonus and in one patient a generalized tonic-clonic convulsion). The side effects coincided with peak Org 6370 serum levels. Our findings indicate that in the photosensitivity model experimental drugs with proven anticonvulsant properties in animals may increase rather than decrease the degree of patient photosensitivity. Photosensitive patients may represent a special subgroup of epileptic patients and therefore need to be classified as such.

Administration, Oral↗

PubMed1982

Molecular aspects of drug photosensitivity with special emphasis on psoralen photosensitization reaction.

Photosensitization reactions involve phototoxic reactions and photoallergic reactions, which are less common. Common drugs and chemicals that photosensitize humans are listed. Phototoxic reactions include the following: 1) direct photosensitization (type I reactions), in which the reactions of the triplet-state sensitizer are directly attributable to a component other than oxygen (e.g., DNA, proteins, and cell membranes), and 2) indirect photosensitization (type II reactions), in which the triplet state of a sensitizer reacts first with molecular oxygen, producing an "active oxygen" intermediate that subsequently reacts with the biologic system. The active oxygen intermediates are singlet oxygen (1O2)k, superoxide radical anions (O(2), and hydroxy radicals. Psoralen-induced skin photosensitization appears to involve both type I and type II reactions. The formation of monofunctional bifunctional psoralen-DNA photoadducts (a type I reaction) is probably responsible for cell damage, cell death, mutation, and even skin carcinogenesis. The erythema response appears to be the result of a type II reaction.

Animals↗

PubMed2003

Secondary reactive oxygen species extend the range of photosensitization effects in cells: DNA damage produced via initial membrane photosensitization.

The type-II photosensitization process is mediated by the formation of singlet oxygen (O2[1deltag]). The short lifetime of this species dictates that chemical reactions with biological substrates can only occur when O2(1deltag) is in very close proximity to the photosensitizer itself. In this study, deuteroporphyrin, a type-II, membrane-localized photosensitizer, was used to generate O2(1deltag) in human lymphoblast WTK-1 cells, and the range of influence was determined by a variety of biological assays. Surprisingly, the initial membrane-confined events were shown, by comet assay, to induce DNA damage in these cells. DNA damage was inhibited both by membrane-localized (alpha-tocopherol acetate) and by cytoplasmic (trolox) free radical scavengers. Comet formation also was inhibited by treatment at low temperature. DNA fragmentation was not influenced by treatment with the pan-caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, showing that apoptosis was not responsible for fragmentation. Taken together, these results show that primary photosensitization reactions involving O2(1deltag), even when tightly confined in extranuclear locations, leads to the production of secondary reactive oxygen species, probably as a result of lipid peroxidation, that can act at greater distances from the photosensitizer itself. These experiments were carried out under conditions where cell survival was significant and raise questions regarding DNA damage and mutagenesis pathways, even when extranuclear O2(1deltag)-generating compounds are used.

Cell Membrane↗

PubMed1986

Mechanisms of contact photosensitivity in mice. VI. Oxygen intermediates are involved in contact photosensitization but not in ordinary contact sensitization.

To investigate the possible participation of oxygen intermediates (OIs) in the contact photosensitization process, mice were treated with long-acting liposomal-superoxide dismutase (L-SOD) before photosensitization. Photosensitization to 3,3',4',5-tetrachlorosalicylanilide (TCSA) was significantly suppressed by the pretreatment of mice with L-SOD. This suppression was not mediated by suppressor cells or due to an unresponsive state produced by the use of L-SOD. Rather, the suppression appeared to be due to the failure of production of photoallergen. L-SOD treatment induced the suppression of contact photosensitivity to TCSA but not ordinary contact sensitivity to TCSA or dinitrofluorobenzene, suggesting that the production of photoallergen is more critically dependent on the presence of OIs than that of ordinary contact allergen. The results provide evidence that OIs are produced by light absorption in the presence of oxygen and react with the biologic substrate to form photoallergens.

Animals↗

PubMed1999

Molecular mechanisms of photosensitization induced by drugs. XII. Photochemistry and photosensitization of rufloxacin: an unusual photodegradation path for the antibacterials containing a fluoroquinolone-like chromophore.

The UVA irradiation of 9-fluoro-2,3-dihydro-10-4'-methyl-1' -piperazinyl-7-oxo-7H-pyrido[1,2,3-de]-1,4-benzo-thiazine-6-carboxylic acid, rufloxacin, a fluoroquinolone antibacterial that shows photosensitizing properties toward biological substrates, leads to formation of two main steady photoproducts characterized by a decarboxylation process and an opening of the piperazinyl ring, respectively. The deprotonation of the 10-piperazinyl group and the dissociation of the 6-carboxyl group of rufloxacin are strictly pH dependent. The photosensitizing activity was tested toward membranes as biological targets. Red blood cell hemolysis and lipid peroxidation were considered as markers of photosensitization. Ultraviolet A-induced damage is strongly influenced by the presence of oxygen, it is triggered by transient species, such as singlet oxygen and free radicals, photogenerated via rufloxacin irradiation, whereas no drug photoproduct is involved in the photosensitization process.

Anti-Infective Agents↗

PubMed1980

Photosensitivity in South Africa. II. The experimental production of the ovine hepatogenous photosensitivity disease geeldikkop (Tribulosis ovis) by the simultaneous ingestion of Tribulus terrestris plants and cultures of Pithomyces chartarum containing the mycotoxin sporidesmin.

The mycoflora of toxic pastures were surveyed during a number of outbreaks of ovine hepatogenous photosensitivity in South Africa. Pure cultures of several isolates were dosed to sheep, but only those of Pithomyces chartarum and Myrothecium verrucaria proved to be toxic. Photosensitization was induced in sheep by dosing them with cultures of a P. chartarum isolate (GA10) obtained from Tribulus terrestris plants collected during an outbreak of geeldikkop in the Karoo. Thus for the first time a mechanism whereby T. terrestris plants can contribute to the causation of ovine hepatogenous photosensitivity was demonstrated. When cultures of GA10 equivalent to approximately 0,75--4,0 mg/kg sporidesmin were dosed at Onderstepoort Veterinary Research Institute to Highveld and Karoo sheep on a diet of lucerne, facial eczema was produced. Dosing the same cultures at levels equivalent to c. 1,0 mg/kg of sporidesmin in the Karoo resulted in lesions characteristic of both facial eczema and geeldikkop. Typical hepatic lesions of geeldikkop could be elicited by dosing GA10 at levels equivalent to c. 0,25--0,7 mg/kg of sporidesmin to Karoo sheep grazing on predominantly T. terrestris pastures in the Karoo. In the latter experiment geeldikkop was induced in the sheep on T. terrestris pastures, while those receiving identical doses on veld with little T. terrestris developed facial eczema. Geeldikkop, therefore, can be brought about by the ingestion of T. terrestris plants together with toxic cultures of P. chartarum. The plant appears not only to act as a vehicle for ingestion of spores, but also to interact with sporidesmin to induce lesions typical of geeldikkop, whereas sporidesmin alone results in facial eczema. Indications are that it can enhance the ability of sporidesmin to cause photosensitivity or, possibly, vice versa. The histopathological findings of these experiments are described in detail.

Animals↗

PubMed1992

Photosensitization by anticancer agents. 11. Mechanisms of photosensitization of human leukemic cells by diaminoanthraquinones: singlet oxygen and radical reactions.

The synthesis of several aminoanthraquinone derivatives (AAQs), designed to suppress the dark toxicity and to promote more efficient cancer cell photosensitization for potential use in photodynamic therapy (PDT), is described. The following AAQs were synthesized: 1-NH2-4,5-(MeO)2-AQ (1), 1,5-(NH2)2-4,8-(MeO)2-AQ (2), 1,8-(NH2)2-4,5-(MeO)2-AQ (3), and 1,5-(NHPhMe)2-4,8-(MeO)2-AQ (8). The agents exhibit strong absorption in the region 480-620 nm. Possible mechanisms of photosensitization were studied by measuring 1O2 phosphorescence at 1270 nm, detecting superoxide radicals employing an electron paramagnetic resonance (EPR)-spin trapping technique, and measuring oxygen consumption during the photo-oxidation of a representative biological electron donor, NADH. Strong phosphorescence from 1O2 was observed upon illumination of 2 and 3 in C6H6 (quantum yield of 0.25 and 0.5 respectively), and in EtOH (quantum yield of 0.23 and 0.34). The 1-amino-AQ (1) was the weakest 1O2 sensitizer, with quantum yield of 0.13 in benzene. No phosphorescence was observed in EtOH. A superoxide radical was detected as a spin adduct of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) in irradiated benzene solutions of 1, 2 or 3 and DMPO. AAQs 2 and 3 sensitized photo-oxidation of NADH in H2O/EtOH mixture with the intermediacy of singlet oxygen as judged by the effect of sodium azide on the photostimulated oxygen consumption. Evolution of O2 upon addition of catalase to the illuminated solution confirmed the ultimate formation of hydrogen peroxide. These findings suggested that the (di)amino-dimethoxyanthraquinones might exert photosensitization via both Type I and Type II mechanisms. The AAQs were tested for their ability to photosensitize K562 human chronic myeloid leukemic cells in culture. Viability was measured using the 3,4,5-diethylthiazol-2,5-diphenyl tetrazolium blue assay, and DNA and possible membrane damage were assessed. The results from illuminating cells with light > 475 nm show that for the 1,5-compounds, the presence of methoxy substituents at 4,8 positions reduces the dark toxicity from ID50 of 23 to 250 microM and for the 1,8-compounds correspondingly from ID50 of 53 to > 300 microM. In the 1,5-series this decrease of the dark toxicity is accompanied by an increase in light-induced dose modification from 8.85 to 14.4. Differences exist in the mechanisms of cytotoxicity between the prototype phenolic AAQs and their methoxy counterparts. It appears that the cytotoxic action of the latter causes cell damage by the formation of a high proportion of alkali labile sites in addition to frank strand breaks.(ABSTRACT TRUNCATED AT 400 WORDS)

Anthraquinones↗

PubMed1994

Evaluation of a new photosensitizer, meso-tetra-hydroxyphenyl-chlorin, for use in photodynamic therapy: a comparison of its photobiological properties with those of two other photosensitizers.

The properties of a new photosensitizer, meso-tetra-hydroxyphenyl-chlorin (mTHPC), were studied using V79 cells (Chinese-hamster lung fibroblasts). Comparisons were made with 2 other photosensitizers: photofrin II (PII) and meso-tetra-hydroxyphenyl-porphyrin (mTHPP). A main advantage of mTHPC is that it has a strong absorption at 652 nm. Maximal cellular uptake of the dye was observed after 24 hr incubation of the cells with the drug. Using a confocal laser-scanning fluorescence microscope, we observed a diffuse distribution of mTHPC in the cytoplasm. Furthermore, the lipophilicity of mTHPC was compared with that of the components of PII by means of high-pressure liquid chromatography (HPLC). Absorption and fluorescence spectroscopy indicated that aggregated as well as monomeric mTHPC was bound to the cells. The action spectrum for photo-inactivation of the cells showed that aggregated mTHPC did not contribute significantly to its photosensitizing effects. In the present cellular system, the efficiency of photodynamic therapy (PDT) with mTHPC (cells were irradiated at a wavelength of 652 nm) was higher than with PII (irradiation at 630 nm) or with mTHPP (648 nm). The quantum yield for photo-inactivation of cells was smaller for mTHPC than for mTHPP and PII. The addition of 1,3-diphenylisobenzofuran (DPBF) reduced cell inactivation during PDT. Thus, PDT with mTHPC seems to act at least partly via a type-II process.

Animals↗

PubMed1995

Adjuvant-induced persistent photosensitivity models in guinea pigs. I. Induction of persistent photosensitivity.

Induction of persistent photosensitivity in guinea pigs was carried out in an attempt to induce a model suitable to clarify the mechanism of human persistent light reactors. Guinea pigs were treated with intradermal injection of adjuvant which consisted of desiccated Mycobacteria followed by topical application of hapten solution and irradiation with UVA. Unequivocal skin reactions were subsequently elicited with UVA exposure in the absence of hapten application. This enhanced UVA reactivity persisted and could be elicited for more than 2 years. In these guinea pigs, remarkably increased sensitivity to UVB was also observed. These animals appear quite similar to persistent light reactors among humans. Muramyl dipeptide used in place of Mycobacteria was also found to be effective in inducing photosensitivity to UVA. There were great differences of reactivity noted among different strains of guinea pig, suggesting that persistent photosensitivity is influenced by genetic background. Enhanced UV sensitivity was induced without hapten application, only with injections of adjuvant and UVA irradiation in the immunization procedure. These results suggest that this model will be useful to study chronic actinic dermatitis.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed1999

Photosensitivity in the Smith-Lemli-Opitz syndrome: the US experience of a new congenital photosensitivity syndrome.

Photosensitivity has been briefly mentioned in several publications on the Smith-Lemli-Opitz (SLO) syndrome, an autosomal recessive mental retardation syndrome. We conducted a questionnaire-based survey to determine the incidence and main features of photosensitivity in SLO. We confirmed a high incidence, and initial evidence suggests that SLO may be the first example of an inherited photosensitivity disorder in which sensitivity to UVA is common.

Adolescent↗

PubMed2001

Nuclear transport of photosensitizers during photosensitization and oxidative stress.

The nuclear transport pathways of the photosensitizers meso-tetra(4-sulfonatophenyl)porphyrin (TPPS4) and meso-tetra(4-N-methylpyridyl)porphyrin (TMPyP) during photosensitization and oxidative stress were characterized in CT-26 murine colon carcinoma cells using fluorescence microscopy and multi-pixel spectral imaging. Prior to irradiation, TPPS4 and TMPyP localized mainly in the lysosomes, while irradiation or H2O2 treatment induced a relocalization into the nucleus and nucleoli. Flow cytometry analysis of isolated nuclei from the treated cells showed an increase in nuclear fluorescence accompanying the relocalization. Isolation and separation of the nuclear proteins according to molecular weight was performed using a sephadex G-100 column. The protein fractions exhibiting high fluorescence were separated by high performance liquid chromatography. Five major classes of proteins with a retention time of 1, 7, 11, 12 and 15 min were obtained. Each photosensitizer was associated with a distinct class of proteins. While TPPS4 fluorescence was detected in the protein fraction with a retention time of 11 min, TMPyP fluorescence was associated with a protein fraction having a retention time of 7 min. We conclude that although oxidative stress triggers entry into the nucleus of both TPPS4 and TMPyP, each sensitizer uses a distinct transport mechanism based on its chemical properties.

Active Transport, Cell Nucleus↗

PubMed1999

Molecular mechanisms of photosensitization XIII: a combined differential scanning calorimetry and DNA photosensitization study in non steroidal antiinflammatory drugs-DNA interaction.

A combined differential scanning calorimetry (DSC) and photosensitization study has been carried out on the interaction of several NSAID on DNA, both from calf thymus and pBR 322 plasmid. The investigated compounds were both non-steroidal anti-inflammatory drugs as well as compounds related to NSAIDs for structural similar properties, to find evidence for their ability to interact with DNA as a function of steric hindrance and polarity of the chemical structures. The considered NSAIDs were diflunisal (DFN, a salicylic derivative), naproxen (NAP), ketoprofen (KPF), suprofen (SPF) and tiaprofenic acid (TIA, arylpropionic acids). The structural criterion used was related to three different aromatic groups, biphenyl, naphthalene and benzophenone (BZP). In fact drug-DNA interaction can be revealed by variations of the enthalpies and temperatures of unfolding of DNA obtained by comparison of calorimetric peaks, where a decrease of the enthalpy is associated with the drug-DNA interaction, by engaging electrostatic bonds. Testing their ability in inducing DNA cleavage when UVA irradiated can evidence the photosensitizing properties of the drug. A good correlation was found between calorimetric and photosensitization studies. From the results obtained it can be reasonably supposed that the photocleavage depends only on the drug molecules bound to DNA.

Animals↗

PubMed1984

Mechanisms of contact photosensitivity in mice. IV. Antigen-specific suppressor T cells induced by preirradiation of photosensitizing site to UVB.

Mice were successfully contact photosensitized with 3,3',4',5-tetrachlorosalicylanilide (TCSA) plus black light irradiation. Pre-exposure of the photosensitizing site (ca 5 cm2) to UVB (280 to 320 nm; 400 mJ/cm2) rendered mice unresponsive to a challenge reaction. Cell transfer experiments demonstrated that the spleens from the nonreactive mice contained suppressor T cells (Ts) that were antigen-specific and that blocked the afferent limb of contact photosensitivity to TCSA. To exert suppressive functions, Ts required another population of cyclophosphamide-sensitive T cells that resided in the spleens of nonsensitized mice. The results provide evidence that UVB-induced aberrant homeostasis of the skin caused a marked suppression of immune system that is associated with the generation of Ts.

Allergens↗