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Objective:To analyze clinical characteristics of cutaneous delayed-type hypersensitivity caused by injection of equine tetanus antitoxin (TAT) or equine anti-tetanus immunoglobulin F (ab′) 2. Methods:Clinical data were collected from 181 outpatients or inpatients with cutaneous delayed-type hypersensitivity caused by injection of equine TAT or anti-tetanus immunoglobulin from 2008 to 2020, and retrospectively analyzed.Results:Before the injection of equine TAT or anti-tetanus immunoglobulin, skin test was negative in 171 (94.47%) of the 181 patients, and the 10 (5.53%) patients with positive skin test responses received desensitization injection. Among the 181 patients, there were 118 males and 63 females aged from 11 to 68 years, with the disease duration of 1 to 7 days and alatency period of 4 to 14 days. There was no significant difference in the clinical manifestations between the patients receiving injection of TAT (130 cases) and those receiving injection of equine anti-tetanus immunoglobulin (51 cases) . Urticaria-like rashes were the main clinical manifestation, and infiltrative erythema occurred at the injection site in 12 patients, of whom 10 developed generalized urticaria all over the body. Of the 181 patients, 163 (90.06%) presented with generalized skin rashes, and 56 (30.94%) had systemic symptoms such as chest tightness, fever, etc, of whom 15 (26.79%) had a history of allergies and 6 with severe symptoms had no history of allergies. Thirty-four (18.78%) patients had single or multiple laboratory abnormalities, such as increased white blood cell counts, elevated C-reactive protein level and urinary glucose, and presence of occult blood in urine. All cases responded well to the treatment with antihistamines and glucocorticoids. The treatment duration ranged from 3 to 10 days, and the outcome was good.Conclusion:TAT-or anti-tetanus immunoglobulin-induced cutaneous delayed-type hypersensitivity may still occur in patients with a negative skin test or after desensitization treatment, and mainly manifests as urticaria-like rashes.
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Objective To evaluate the effect of RNA interference in p53 gene on the expressions of genes involved in ultraviolet B (UVB)-induced premature senescence and photocarcinogenesis in human skin fibroblasts (HSFs).Methods A previously established HSF cell clone with repressed expression of p53,which was named as HSF-p53,was cultured and irradiated with a subcytotoxic dose (10 mJ/cm2) of UVB once a day for five consecutive days.The HSFs with normal expression of p53 served as the control.Subsequently,β-galactosidase (SA-β-gal)-staining was performed to estimate the degree of senescence,quantitative real-time PCR array was performed to determine the mRNA expressions of photocarcinogenesis-and senescence-associated genes,including p53,p21,p19,p16,pRb,fibronectin,osteonectin,smooth muscle 22 (SM22),bax,bcl-2,hypoxia-inducible factor-1 α (HIF-1α),vascular endothelial growth factor(VEGF),and human double minute-2 (hdm2).Statistical analysis was carried out by Student's t test using the software SPSS 10.0.Results The percentage of SA-β-gal-positive cells in irradiated HSF-p53 was 19.70％ ± 0.85％,significantly higher than that in unirradiated HSF-p53 (12.77％ ± 0.81％,t =6.45,P ＜ 0.05),but lower than that in irradiated control HSFs (50.48％ ± 5.30％,t =7.86,P ＜ 0.05),and similar to that in unirradiated control HSFs (18.50％ ± 0.45％,t =2.57,P ＞ 0.05).Compared with the control HSFs,the HSF-p53 showed decreased expressions of p21,p19,fibronectin,osteonectin,SM22 and bax genes (all P ＜ 0.05),but increased expressions of bcl-2,HIF-1α,VEGF and hdm2 genes (all P ＜ 0.05),and a similar expression of p16 gene (P ＞ 0.05); the repeated UVB radiation significantly promoted the expressions of p16 and pRb genes (both P ＜ 0.05),but had no obvious effect on the expressions of the other genes in HSF-p53 compared with unirradiated HSF-p53 (all P ＞ 0.05).Conclusions The inhibition of p53 expression may decelerate the UVB-induced premature senescence in HSFs,which may be involved in the p53-dependent tumor suppression.
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Objective To assess the expression pattern of protease-activated receptor 2 (PAR2) in human keratinocytes and to characterize its biological functions in the regulation of skin barrier.Methods Primary human keratinocytes and human N/TERT keratinocytes were used as the subject of this study.The expression and distribution of PAR2 in the keratinocytes were analyzed by using immunoflorescence staining and Western blot.Two different PAR2 agonists,trypsin and a PAR2-activating peptide (AP),as well as a PAR2-antagonistic peptide (H2N-FSLLRY-COOH) and a control peptide were used to induce the activation of PAR2 in the keratinocytes.Then,a fluorescence-based calcium mobilization assay was performed to evaluate the biological function of PAR2.Data were statistically analyzed by one-factor analysis of variance.Results Under normal culture conditions,PAR2 was weakly expressed in keratinocytes,and the expression was unaffected by culture medium composition or culture duration.Calcium mobilization was induced by trypsin of 50-250 nmol/L and the PAR2-activating peptide in a dose-and time-dependent pattern.The maximal activation of PAR2 was observed in keratinocytes treated with the PAR2 agonist HAN-SLIGKV-COOH of 75-250 μmol/L.The PAR2-antagonistic peptide (H2N-FSLLRY-COOH) obviously suppressed the increase in calcium mobilization induced by trypsin,while the control peptide PAR-RAP showed no inductive effect on the PAR2 activation based on the absence of calcium mobilization.The substrate-induced calcium release was complete within 250 seconds,and peaked at 50 seconds after the initial trypsin or PAR-AP stimulation.Moreover,the activation of PAR2 was accompanied by an increase in ERK phosphorylation and elicitation of MAPK signaling pathway in keratinocytes.Conclusions Human keratinocytes positively express PAR2,which can be activated by trypsin and PAR2-activating peptides,and the activation of PAR2 may influence the physiological function of keratinocytes by inducing intracellular calcium release.
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Objective To establish a cell line with repressed expression of p53 by transfecting a plasmid construct expressing short hairpin RNA(shRNA)targeting p53 into human skin fibroblasts(HSFs),and to evaluate the effect of repression of p53 expression on the senescence in HSFs.Methods The eukaryotic expressing plasmid pGCsi-p53 containing shRNA targeting p53 gene was transfected into HSFs with lipofectamine.Subsequently,the cells were selected by G418,and resistant cell clones were chosen and expanded.Reverse transcription-PCR and real time fluorescence-based quanitative PCR were performed to determine the expression of p53 gene,and Western blot to detect the expression of p53 protein in HSFs.The senescence in HSFs was evaluated by SA β-gal staining,and cell proliferation by methyl thiazolyl tetrazolium(MTT)assay.Results A HSF clone with repressed expression of p53 was established successfully.The expressions of p53 mRNA and protein were downregulated in transfected HSFs compared with untransfected HSFs(0.09 ± 0.03 vs.0.32 ± 0.04,0.11 ± 0.04 vs.0.84 ± 0.05,both P ＜ 0.01).The percentage of senescent cells was 13.47％ ± 1.01％ in the transfected HSFs,significantly lower than that in untransfected HSFs(18.10％ ± 0.66％,P ＜ 0.05).As MTT assay showed,the proliferation was accelerated in transfected HSFs compared with untransfected HSFs(P ＜ 0.05).Conclusions The repression of p53 expression decelerates the senescence in HSFs,but promotes the proliferation of HSFs.
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Objective To study the protective mechanism of astragaloside on skin photoaging. Methods BALB/c mice were randomly divided into four groups: model group irradiated with ultraviolet rays (UV), model plus matrix group pretreated with the matrix before UV irradiation, model plus astragaloside group pretreated with astragaloside 0.08% cream before UV irradiation, normal control group received no irradiation or pretreatment. After 4-week irradiation, the mice were sacrificed, and skin tissues were resected from the back of these mice. Then, reverse transeription PCR (RT-PCR) and immunohistochemistry were performed to detect the mRNA and protein expression of TGF-βR Ⅱ and Smad 7, respectively. Gray scale ratio was used to represent the mRNA levels of TGF-βR Ⅱ and Smad 7. Results There was a significant difference in the mRNA level (F = 80.98, 736.80, respectively, both P 0.01). Conclusion Astragaloside can prevent skin photoaging by the alteration of TGF-β pathway via up-regulating TGF-βR Ⅱ expression and down-regulating Smad 7 expression.
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Objective To explore the influences of extracellular matrices (ECM) secreted by ultraviolet B (UVB)-induced senescent fibroblasts on the proliferation of and extracellular signal-regulated kinase (ERK) signaling in HaCaT cells. Methods Fibroblasts were irradiated with UVB of 15 mJ/cm2 once daily for 5 days to induce premature senescence, which was identified by SA-β-gal staining 72 hours after the last irradiation.HaCaT cells were divided into 3 groups and inoculated into plates coated with extracellular matrices secreted by non-senescent (PRE-ECM) or senescent fibroblasts (SIPS-ECM) or into uncoated plates (NON-ECM), fol-lowed by additional culture. U0126, an inhibitor of ERK1/2, was used to treat the HaCaT cells 1 hour before inoculation. Then, MTT assay was carried out to detect the proliferation of HaCaT cells after a 3-day culture,Western blot to assess the phosphorylation of ERK at 0.5, 1, 2 and 4 hours after the inoculation, flow cytometry to analyse cell cycle and apoptosis after 24 hours of culture. Results The most rapid and intense phosphory-lation of ERK was observed in SIPS-ECM group. Inhibiting the activation of ERK pathway with U0126 could completely suppress the promoting effect of ECM from senescent fibroblasts on the proliferation of HaCaT cells.After the blocking of ERK activation, the proportion of HaCaT cells in S and G2/M phase decreased from 37.40%, 41.34% and 43.31% to 29.41%, 36.48% and 39.96%, respectively, in NON-ECM, PRE-ECM and SCIP-ECM group. Conclusion The ECM produced by UVB-induced senescent fibroblasts promote the prolifera-tion of HaCaT cells via inducing the phosphorylation of ERK.
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Objective To observe the expressions of senescence-associated biomarkers in fibroblasts after repeated exposures to subtoxic doses of ultraviolet B (UVB), and to study the effect of ginsenoside Rb1 and Rg1 as well as Lycium barbarum polysaccharide on the UVB-induced premature senescence and on the expressions of senescence-associated signals including pl6, p21 and pS3. Methods Skin fibroblasts were classified into 8 groups to receive pretreatment with traditional Chinese medicine (TCM) monomers only, UVB irradiation only, no treatment, or both pretreatment and irradiation. UVB was given successively at a dose of 15 mJ/cm~2 for 10 times, and the concentration of three monomers was 50 mg/L. After 5 days of treatment, light microscopy was used to observe the morphology of fibroblasts, transmission electron microscopy to study the cell ultrastructure,β-galactosidase histochemical staining to detect senescent cells, flow cytometry to analyze cell cycle, and RT-PCR to measure the mRNA expressions of p16, p21 and p53 in these skin fibroblasts. Results None of the 3 monomers had any effect on cell morphology, P-galactosidase activity, cell cycle or the mRNA expression of p53, p21 and pl6 in skin fibroblasts. After UVB irradiation, some changes occurred to cell morphology and ultrastructure; 91.5% of the cells were stained positively for P-galactosidase. The proportion of cells in G1 phase was 88.63% ± 4.67% in irradiated fibroblasts, significantly different from that in untreated controls (49.18% ± 5.53%, P< 0.05) and that in irradiated fibroblasts pretreated with ginsenoside Rbl and Rgl as well as Lycium barbarum polysaccharide (71.04% ± 1.64%, 70.38% ± 2.58%, 80.09% ± 3.46%, all P < 0.05). Compared with untreated fibroblasts, the mRNA expression of p53, p21 and pl6 significantly increased in irradiated fibroblasts (P < 0.05), however, the induced increase in the mRNA expression of pl6 was inhibited by all the three monomers (all P< 0.05), that of p2l by ginsenoside Rb1 and Rg1 (P< 0.05), and that of p53 by ginsenoside Rbl and Lycium barbarum polysaccharide (both P < 0.05). Conclusions Ginsenoside Rbl, Rgl and lycium barbarum polysaccharide can inhibit UVB-induced premature senescence, which may be associated with the down-regulation of mRNA expressions of pl6, p21 and p53.
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ngthen cellular immunity, especially Th1-type immune response to HPV11-E7 DNA vaccine in mice.
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Objective To study the effects of the IL-1 receptor antagonist (IL-1Ra) on matrix metalloproteinase 1 (MMP-1) expression in UV-irradiated fibroblasts. Methods Simulating the impact of environmental ultraviolet (UV) light on human skin, UVA-irradiated human fibroblasts were cultured in medium obtained from UVB-irradiated HaCaT cells. MMP-1 was detected by ELISA in the culture medium of fibroblasts. After treatment with IL-1Ra, the mRNA expression levels of C-Jun, C-Fos and GAPDH (internal control) of fibroblasts were measured by real-time fluorescent quantitative RT-PCR. Results Production of MMP-1 by UVA (10 J/cm2)-irradiated fibroblasts was increased in culture medium from UVB-irradiated HaCaT cells. The fibroblasts produced significantly higher levels of MMP-1 in culture medium from HaCaT cells treated without UVB than those with 15 mJ/cm2 UVB (t = 8.413,P= 0.014). However, IL-1Ra inhibited MMP-1 production of fibroblasts in a dose-dependent manner. Standard curves of real-time fluorescent quantitative RT-PCR showed a linear correlation between the copy number and the threshold cycle (Tc). Melting curves confirmed the specificity of PCR products. The original copy numbers of C-Jun and C-Fos as well as the ratios of the numbers to the GAPDH copy number showed that IL-1Ra inhibited the C-Jun mRNA expression of fibroblasts in a dose-dependent manner but had no significant effects on C-Fos mRNA expression. Conclusions The culture medium from UVB-irradiated HaCaT cells can promote MMP-1 production by UVA-irradiated fibroblasts. IL-1Ra reduces MMP-1 production via inhibition of C-Jun mRNA expression.
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Objective To determine the potential impact of superantigens produced by skin-colonizing Staphyiococcus aureus in patients with atopic dermatitis and eczema. Methods Of 117 patients with atopic dermatitis and 199 with eczema, 140 Staphyiococcus aureus strains were isolated from the skin specimens. Superantigens were detected with reverse passive latex agglutination. Results Among 140 Staphyiococcus aureus strains, 60 (42.9%) produced superantigens, among which 43 produced one kind of superantigens only and 17 produced at least two kinds. Of strains isolated from atopic dermatitis, 51.5% produced superantigens and no significant difference was seen in superantigen production between lesional and non-lesional strains in atopic dermatitis. Of strains isolated from eczema patients, 34.7% (all were lesional strains) produced superantigens. The positive rates of total superantigens, lesional superantigens and toxic shock syndrome toxin-1 production were all higher in the strains from atopic dermatitis than in those from eczema. Conclusions Superantigen production by skin-colonizing Staphyiococcus aureus probably plays a more important role in atopic dermatitis than that in eczema. However, further studies are necessary to validate its importance.
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Objective To investigate the protective effect of aloin on inducible nitric oxide synthase (iNOS) and nuclear factor kappa B (NF-kB) synthesis of HaCat cells induced by ultraviolet B (UVB) irradiation. Methods The proliferation of HaCat cells was measured by MTT method. iNOS mRNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR). NO production was assessed by spectrophotometric method, and expression of NF-kB P65 was measured by immunofluorescent staining. Results After irradiation with 30 mJ/cm~2 of UVB, proliferation of HaCat cells was decreased, and NO generation and iNOS mRNA synthesis in HaCat cells were increased. UVB irradiation could also activate the expression of NF-kB P65 and promote its translocation into nucleus. NO generation and iNOS mRNA synthesis were markedly down-regulated in a dose-dependent manner by pre-treatment with different concentrations of aloin. The activation of NF-kB P65 was inhibited while the proliferation of HaCat cells was increased. All the difference reached statistical significance (P
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Objective To investigate the efficacy and safety of butenafine hydrochloride 1% aerosol in the treatment of tinea pedis,tinea cruris or tinea corporis.Methods A randomized,double-blind,multi-center clinical trial was conducted.Efficacy was assessed in terms of mycological cure,total clinical sign and symptom scores,and clinical response,at baseline,mid-term,end of study,and 2 weeks after treatment.Results One hundred and seventeen patients with tinea cruris or tinea corporis were randomly allocated to individual groups treated with either butenafine 1% aerosol (n = 58,male 53,female 5,age 29.45 ? 11.80,course of disease 3.0 ? 5.0 months) or bifonazole 1% aerosol (n = 59,male 49,female 10,age 34.12 ? 12.98,course of disease 3.0 ? 11.0 months).One hundred and nineteen patients with tinea pedis were also allocated to two groups treated with either butenafine (n = 59,male 59,age 22.97 ? 3.97,course of disease 24.0 ? 36.0 months) or bifonazole (n = 60,male 60,age 23.77 ? 4.12,course of disease 36.0 ? 48.0 months).The cure rates and total response rates were 25.86% vs.40.68%,and 86.21% vs.91.53%,in the study group and the control group,respectively,at the end of study,and 58.62% vs.74.58%,and 96.55% vs.96.61% in 2 weeks following-up,for the patients with tinea cruris or tinea corporis.Also,the cure rates and total response rates were 23.73% vs.25.00%,81.36% vs.78.33%,in the study group and the control group,respectively,at the end of study,and 37.29% vs.41.57% and 81.36% vs.90.00% in 2 weeks following-up,for the patients with tinea pedis.Local adverse reactions were recorded in 13 of butenafine group,and 20 of bifonazole group.The differences of above data between two groups were not statistically significant.Conclusion Butenafine hydrochloride 1% aerosol is effective and well tolerated for the treatment of tinea pedis,tinea cruris or tinea corporis.
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Objective To elucidate the correlation between the dose of ultraviolet B (UVB) irradiation and apoptotic phase of keratinocytes (HaCaT cells). Methods Cultured immortalized human ker-atinocyte cell line, HaCaT cells, was irradiated with ultraviolet B (UVB) in doses of 20, 40, 60, 80, 100 and 120 mJ/cm2. Cellular viability, cell cycles and apoptosis were simultaneously detected at 2, 12, 24, 48 and 72 h after irradiation. The caspase-mediated apoptosis was detected by FITC-labelled VAD-FMK, which could irreversibly bind to activated caspases. FITC-Annexin V and PI double staining detected cell membrane-mediated apoptosis. Cell nucleus-mediated apoptosis was detected by DNA ladder electrophoresis. Results Cell cycle analysis revealed that UVB treated HaCaT cells were blocked predominantly in G2/M phase in a dose-dependent manner. Treatment with UVB decreased the viability of HaCaT cells in dose- and time-dependent manners. The rates of apoptosis were increased with increasing dose and prolongation of time after UVB irradiation. The apoptosis of UVB-treated HaCaT presented in an obvious time-dependent manner, in which caspase- and cell membrane-mediated apoptosis was predominantly in early phase and cell nucleus-mediated apoptosis predominantly in late phase. Conclusions The apoptosis of UVB treated HaCaT cells appears in dose- and time-dependent manners, which warrants further detection with multiple parameters and at different phases.
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Objective To study the bacteriological characteristics and the pathogenesis of Staphylococcus aureus (S. aureus) on eczema and atopic dermatitis (AD). Methods A multi-center randomized, double blind bacteriological study on the lesions and non-lesional skin of patients with eczema (207) and AD (119) were carried out. The antibiotic sensitivity and the bacteriophage typing were performed on all the S. aureus isolated from the patients. Results There were statistical differences in the positive rate of the culture, the ratio and the colonization of S. aureus between the lesion and the non-lesional skin in eczema (P
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Objective To explore the inhibitory action of antisense c-jun oligodeoxynucleotides(ODN) on matrix metalloproteinase(MMP) expression of fibroblasts induced by ultraviolet B (UVB). Methods The c-jun and c-fos protein expression induced by UVB were measured by Western blot. The mRNA expression of c-jun was determined by reverse transcriptase polymerase chain reaction (RT-PCR) after transfection with c-jun antisense ODN. The pro-MMP-1 and MMP-3 synthesis of fibroblasts was measured by ELISA after treatment with UVB and antisense c-jun ODN. Results The UVB-induced c-jun protein expression of fibroblasts increased to 1.8, 2.6, 3.3 times compared with that of non-irradiated controls,while there was no significant change in c-fos protein expression. The pro-MMP-1 and MMP-3 synthesis induced by UVB irradiation increased obviously. After transfection with different concentrations of c-jun antisense ODN, the UVB-induced c-jun mRNA expression could be significantly inhibited(P
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Objective To investigate the colonization features of Staphylococcus aureus (S. aureus) in the skin lesions of eczema and atopic dermatitis (AD), and to evaluate the therapeutic effect of combination topical treatment with mupirocin and hydrocortisone butyrate. Methods A multicentre, double-blind randomi-zed trial was conducted. The SCORAD was evaluated on day 1, 7, 14 and 28. Swabs for bacterial isolation were taken from the lesional skin and non-lesional skin. A combination topical therapy with mupirocin ointment and hydrocortisone butyrate ointment was used in treatment group, with vehicle ointment and hydrocortisone butyrate ointment as a control. Results Three hundred and twenty seven patients were enrolled in the study, including 208 patients with eczema and 119 patients with atopic dermatitis. Bacteria were isolated from 70.19% of lesional skin and 32.69% of non-lesional skin of patients with eczema, in which S. aureus accounted for 47.26% and 27.94% respectively. Bacteria were isolated from 74.79% of the lesional skin and 34.45% of non-lesional skin of patients with atopic dermatitis, in which S. aureus accounted and 79.78% or 80.49% respectively. The amount of S. aureus colonized was markedly higher in the lesional skin than that in non-lesional skin, either in eczema patients or in atopic dermatitis (P 0.05). Conclusions The bacterial colonization, especially S. aureus, is more frequently dectected in the lesional skin of eczema patients and AD patients than that in the non-lesional skin, which may be related in the pathogenesis of eczema and AD. And, early application of combination therapy with topical antibiotics and corticosteroids is beneficial to the patients.
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Objective To evaluate the cumulative irritative effect of topical retinoic acid preparations on normal skin.Methods A randomlized,doubled blind,placebo-controlled clinical trial was carried out with7groups for6tested preparations.All subjects were patch tested with each preparation for24hours on Monday to Thursday,and for72hours on Friday.The patch tests were performed for3consecutive weeks.Results The minimal cumulative irritative effects were found in Group G treated with0.1%adapalene gel,with a cumulative irritative index of0.09?0.11in20days.The cumulative irritative index was significantly lower in Group G than that in Group B treated with0.1%retinoic acid(Diweishuang誖)(0.59?0.24),or in0.025%retinoic acid(Diweishuang誖)(0.41?0.22),or in0.05%retinoic acid(VITAMIN誖Cream)(0.25?0.22).Conclusion Adapalene,the third generation of retinoic acid,is characterized by lower irritative ef-fects in comparison to the first generation of topical retinoic acid agents.
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0.25)levels in the two groups.In the group treated with42mJ/cm 2 UVB irradiation followed by the addition of EGCG,the numbers of apoptotic and dead cells and Fas mRNA were decreased,but bcl-2protein was increased.Conclusions Low dosage of UVB irradiation could induce apoptosis of keratinocytes.High dosage of UVB irradiation might result in cell death.EGCG could reduce UVB-induced apoptosis of keratinocytes by increasing bcl-2protein and decreasing Fas mRNA.
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Objective To observe the clinical efficacy and safety of5%imiquimod cream in the top-ical treatment of condyloma acuminatum(CA).Methods A randomized,double-blind,parallel placebo-controlled clinical study was conducted.The test drug was topically used in CA patients,three times a week for8weeks.Patients whose warts cleared completely were followed up for one month to determine recurrence rates.Results Two hundred fifty-eight patients with anogenital warts were enrolled into this trial.One hun-dred twenty-nine patients were randomly selected to receive5%imiquimod cream;129patients were ran-domly chosen to receive placebo cream.Results showed that the cure rates were12.30%,32.79%,50%,60.66%respectively in study group for2,4,6,8weeks and were4.88%,14.63%,19.51%,26.02%respec-tively in control group for2,4,6,8weeks(P
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Objective To study the immunosuppression mechanism induced by ultraviolet (UV) and cis-urocanic acid. Method The auto lymphocyte proliferation test with Langerhans＇ cell (LC) in guinea -pig was performed. Results In exposure to low dose of UVB (25 J/m2) radiation, the inhibition rate of lymphocyte proliferation stimulated by LC was 10. 5%, the inhibition rates of UVB radiation in doses of 50 J/m2 and 100 J/m2 were 22.4% or 50%, respectively. The lymphocyte proliferation was almost completely suppressed by200J/m2 UVB radiation, while the inhibition of LC function by cis-urocanic acid was weak. Conclusion UVB significantly inhibits LC auto -stimulation in dose -dependent way, which may play an important role in UVB induced immunosuppression.