白癜风患者表皮角质形成细胞凋亡及其与表皮片移植疗效的关系

目的 探讨稳定期白癜风患者皮肤角质形成细胞(KC)的凋亡与表皮片移植疗效的相关性.方法 取44例稳定期白癜风患者的正常腹部皮肤和白斑区皮肤,采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记技术(TUNEL)检测KC的凋亡状况,同时采用免疫组化法检测28例稳定期白癜风患者KC凋亡相关蛋白Caspase 3、8、9及bcl-2、P53的表达情况.结果 TUNEL结果显示,皮损区阳性细胞数与供皮区皮肤相比差异有统计学意义.免疫组化结果:阳性反应定位于KC的胞膜与胞质,阳性细胞主要分布于表皮的中下层.白斑区Caspase 3有19例表达为阳性,而供皮区皮肤为9例.白斑区Caspase 8和9的阳性表达分别为15和16例,供皮区皮肤分别为5和4例.P53在两组标本中的表达都为阴性;Bcl-2在皮损区为阴性,供皮区皮肤中表达为弱阳性.表皮片移植失败组供皮区皮肤中凋亡的KC数目(15.83±2.69)明显多于移植成功组供皮区皮肤(9.24±1.80).结论 白癜风患者皮损区KC凋亡比供皮区皮肤明显,凋亡相关蛋白Caspase 3、8、9表达升高.KC凋亡可能与移植疗效存在一定的相关性.     

Less keratinocyte-derived factors related to more keratinocyte apoptosis in depigmented than normally pigmented suction-blistered epidermis may cause passive melanocyte death in vitiligo

Stem cell factor (SCF) of keratinocyte origin regulates melanocyte growth and survival. Deprivation of survival factors causes the apoptosis of melanocytes. Vitiligo often develops following physical trauma, even if this is minor. The exact mechanism of the Koebner phenomenon in vitiligo is unclear. Apoptosis of keratinocytes, which occurs more in depigmented suction-blistered epidermis than in the normally pigmented counterpart, could reduce levels of keratinocyte-derived factors such as SCF and basic fibroblast growth factor (bFGF). Levels of SCF expression were examined in the depigmented and normally pigmented paired epidermis of 19 patients with vitiligo, and bFGF expression in six patients. The expression of SCF (p<0.001) and bFGF was usually reduced in the depigmented compared with the normally pigmented epidermis. Apoptosis of cultured normal human keratinocytes, which was induced by staurosporine, resulted in a concentration-dependent decrease in levels of SCF mRNA and protein. Normal human melanocytes proliferated more in medium containing SCF or keratinocyte (XB-2) feeder than in medium with neither. Deprivation of SCF or keratinocyte feeder in the culture medium induced a marked decrease in melanocytes as a result of apoptosis. Therefore, lower expression of keratinocyte-derived factors, including SCF, in vitiliginous keratinocytes, which could result from keratinocyte apoptosis, might be responsible for passive melanocyte death and may explain the Koebner phenomenon.     

Role of Keratinocytes in the Development of Vitiligo

Vitiligo is an acquired depigmentary disorder of the skin that results from the loss of functioning epidermal melanocytes. Most studies on vitiligo have concentrated on the abnormality of melanocytes rather than the abnormality of keratinocytes; however, epidermal melanocytes form a functional and structural unit with neighboring keratinocytes. In fact, direct cell-to cell contact stimulates in vitro proliferation of melanocytes, and growth factors produced by adjacent keratinocytes regulate the proliferation and differentiation of melanocytes. The potential role of keratinocyte-derived cytokines has also been presented. We focused on the structural changes in vitiliginous keratinocytes, which may result in loss of melanocytes, to examine the pathomechanism of vitiligo. The results of a comparison between depigmented and normally pigmented epidermis in patients with vitiligo showed that the keratinocytes in the depigmented epidermis were more vulnerable to apoptosis. Impaired Phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase (Akt) activation followed by reduced nuclear factor-κB activation under increased tumor necrosis factor-α levels was demonstrated as a mechanism for keratinocyte apoptosis. The role of aquaporin 3 in keratinocyte apoptosis was addressed based on the relationship between the PI3K/AKT pathway and the E-cadherin-catenin complex. Apoptotic keratinocytes induced a lower expression of keratinocyte-derived factors, including stem cell factor, in depigmented epidermis, resulting in passive melanocyte death.     

Impaired PI3K/Akt activation-mediated NF-kappaB inactivation under elevated TNF-alpha is more vulnerable to apoptosis in vitiliginous keratinocytes

Levels of the cytokines IL-6, IL-1alpha, and tumor necrosis factor-alpha (TNF-alpha) are significantly higher in lesional than in non-lesional skin of patients with vitiligo. However, how cytokines affect pigmentation is not fully understood. To examine the mechanism, Western blot analysis with TNF-alpha, Fas ligand (FasL), and downstream signaling molecules such as I-kappaB, NF-kappaB, TNF-R1-associated factor 2, Akt, and PTEN (phosphatase and tension homologue) were performed for the suction-blistered depigmented and normally pigmented epidermis from 10 patients. Levels of TNF-alpha and FasL were significantly higher in the depigmented epidermis. Interestingly, phosphorylation levels of I-kappaB, NF-kappaB, and Akt were lower in the depigmented epidermis. Moreover, PTEN, which could inhibit the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, was significantly higher in depigmented epidermis, implying that vitiliginous keratinocytes may be more susceptible to TNF-alpha-mediated apoptosis through impaired Akt and NF-kappaB activation. To test this hypothesis, cultured normal human keratinocytes were treated with TNF-alpha in the presence of a PI3K inhibitor to suppress Akt activation. Keratinocytes showing impaired Akt activation demonstrated increased apoptosis with less activation of NF-kappaB. Thus, reduced activation of NF-kappaB via impaired PI3K/Akt activation under increased TNF-alpha levels could result in increased apoptosis of vitiliginous keratinocytes.     

Histamine effect on melanocyte proliferation and vitiliginous keratinocyte survival

Repigmention of vitiligo requires melanocyte proliferation and migration. Keratinocytes have been shown to play a role in this process. Data from this laboratory showed that bee venom (BV) stimulated melanocyte proliferation and migration as well as melanogenesis. As histamine release is associated with BV, its effect on melanocyte proliferation and migration was examined. Cultured normal human melanocytes treated with histamine were studied with and without receptor-specific antagonists or agonists. The effect of histamine on vitiliginous keratinocytes, in cultured cells treated with a PI3K inhibitor in the presence of TNF-α, was also examined. Histamine exerted a more significant effect on melanocyte proliferation than on melanogenesis. This occurred through the H2 receptor with complex signalling to ERK, CREB, and Akt activation, which stimulated melanocyte migration. Histamine and the H2 receptor agonist also increased survival of vitiliginous, but not normal, keratinocytes, with NF-κB activation. Because expression levels of the H2 receptor was significantly decreased in depigmented compared to normally pigmented epidermis, in patients with vitiligo, histamine may increase the survival of vitiliginous keratinocytes. Overall, histamine stimulated the proliferation and migration of melanocytes and the vitiliginous keratinocyte survival, providing the basis for novel therapeutic approaches to vitiligo repigmentation.     

Evaluation of cell death and proliferation in psoriatic epidermis

BACKGROUND: Previous studies of psoriatic epidermis using the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL) method, a type of apoptotic detection method, showed that TUNEL-positive keratinocytes were abundantly distributed in all layers of the psoriatic epidermis, although psoriasis is a hyperproliferative disorder. OBJECTIVE: We sought to clarify the nature of cell kinetics in a psoriatic epidermis on the basis of differences in the reactivities in TUNEL and formamide-induced DNA denaturation assay combined with the detection of denatured DNA with a monoclonal antibody (MAb) against single-stranded DNA (formamide-MAb assay) between the normal and psoriatic epidermides. METHODS: The kinetics of keratinocytes was evaluated by the immunohistochemistry of Ki-67 for proliferation activity and by TUNEL, TUNEL combined with transmission electron microscopy (TUNEL/TEM), and formamide-MAb assay for apoptosis. RESULTS: The number of Ki-67-positive cells in the psoriatic epidermis was significantly higher than that in the normal epidermis. In the normal epidermis, both TUNEL and formamide-MAb assay showed a similar distribution pattern, that is, both TUNEL and formamide-MAb assay-positive keratinocytes were present only in the upper granular layer. In the psoriatic epidermis, most keratinocytes were negative for the formamide-MAb assay, while TUNEL-positive cells were abundantly distributed in all layers of the psoriatic epidermis. TUNEL/TEM method clearly demonstrated that many immunogold particles that stain the sites of 3'-OH DNA ends were evenly distributed on the euchromatin in psoriatic keratinocyte nuclei, in contrast to their presence on the peripheral condensed chromatin in normal keratinocyte nuclei. CONCLUSION: The increased TUNEL reactivity in psoriatic lesions is due to the increase in the number of DNA nicks resulting from active DNA replication but not due to DNA double-strand breaks produced during the apoptotic process, and the formamide-MAb assay is a reliable method for the detection of apoptosis, particularly in the epidermis.     

Reduced expression of the antiapoptotic proteins of Bcl-2 gene family in the lesional epidermis of patients with Darier's disease

BACKGROUND: Dyskeratotic cells in Darier's disease (DD) are thought to represent apoptotic keratinocytes. Bcl-2 gene family proteins play a major role in the regulation of apoptosis of epidermal keratinocytes and reveal pleiotropic interactions with intracellular Ca2+ homeostasis. The latter is impaired in DD because of mutations of ATP2A2 gene that encodes the type 2 isoforms of the sarcoplasmic/endoplasmic reticulum (ER) Ca++ ATPase 2 (SERCA2) pump. METHODS: The expression of Bcl-2, Bax, and Bcl-x(L) proteins was investigated in the epidermis of 11 patients with DD and of 11 sex- and age-matched healthy controls by immunohistochemistry. RESULTS: The expression of Bcl-2 and Bcl-xL was clearly reduced in the lesional epidermis of the patients, as compared with the normal epidermis of healthy controls, whereas the expression of Bax remained unaltered. CONCLUSIONS: The alterations in the expression of Bcl-2 gene family proteins could be a crucial event for the activation of the apoptotic process in the lesional epidermis of DD patients and for the occurrence of the characteristic dyskeratotic keratinocytes. The question as to whether these alterations are associated with the ER Ca2+ depletion in DD or represent secondary phenomena unrelated to the genetic defect of this genodermatosis remains to be elucidated.     

Aberrant expression of apoptosis-related molecules in psoriatic epidermis

Apoptosis is a physiological form of cell death that is responsible for the deletion of cells. Epidermal keratinocytes are supposed to be regulated by cell proliferation and cell death leading to structural homeostasis. Psoriatic skin shows marked thickening of the epidermis, suggesting the imbalance of the homeostasis, which might be related to abnormal apoptotic process. We investigated the expression of various apoptosis-related molecules in the psoriatic hyperproliferative epidermis. Real time quantitative RT-PCR analyses revealed that mRNAs of Fas, Bcl-xL, Bax and ICAD (inhibitor of caspase 3-related DNase) of the psoriatic involved epidermis were increased by 4.2-, 2.8-, 2.6- and 5.6-fold, respectively, compared with the uninvolved epidermis. In contrast, Bcl-2 expression in the involved epidermis was one-third suppressed compared with the uninvolved epidermis. No significant difference in the expression of mRNAs of Fas ligand or CAD (caspase 3-related DNase) was detected between the involved and uninvolved epidermis. Western blot analysis and immunohistochemical studies showed compatible results obtained by RT-PCR analyses. Although active caspase 3 was slightly increased in the involved epidermis, apoptotic cells were marginally detected. These results indicate that psoriatic epidermis shows aberrant expression of apoptosis-related molecules representing suppressed apoptotic process, which might be related to characteristic histopathology.     

Irritancy of dithranol in normally pigmented and depigmented skin of patients with vitiligo

In order to ascertain the extent to which the pigmentary system plays a protective role in dithranol-induced irritancy, a within-subject comparison was carried out between normally pigmented and depigmented skin of patients with vitiligo. In open patch tests, various concentrations of dithranol in a cream base were applied to the normally pigmented and depigmented skin of 6 patients with vitiligo. The responses were assessed 48 h after application. A mild to moderate inflammation occurred in the pigmented and depigmented skin and no statistically significant difference was shown between the two test areas. The present study does not support the hypothesis that the pigmentary system might be involved in dithranol-induced irritancy.     

Effects of Finasteride on Apoptosis and Regulation of the Human Hair Cycle

BACKGROUND: A number of studies have provided evidence that apoptosis is a central element in the regulation of hair follicle regression. In androgenetic alopecia (AGA), the exact location and control of key players in the apoptotic pathways remains obscure. OBJECTIVE: In the present study, we used a panel of antibodies and investigated the spatial and cellular pattern of expression of caspases and inhibitors of apoptosis (IAPs), such as XIAP and FLIP, in men with normal scalp and in men with AGA before and after 6 months of treatment with 1 mg oral finasteride treatment. METHODS AND RESULTS: Constitutive expression of caspases-1, -3, -8, and -9 and XIAP was detected predominantly within the isthmic and infundibular hair follicle area, basilar layer of the epidermis, and eccrine and sebaceous glands. AGA-affected tissues showed an increase in caspase (-1, -3, -6, -9) immunoreactivity with a concomitant decrease in XIAP staining. After 6 months of finasteride treatment, both caspases and XIAP were similar to levels exhibited by normal subjects. Immunoblot analysis was performed to determine antibody specificity and cellular expression of caspases. Purified populations of keratinocytes, melanocytes, dermal papilla, and dermal fibroblasts derived from human hair follicles were cultured in vitro and treated with 0.5 mm staurosporin. Time-course experiments revealed that processing of caspase-3 is a principal event during apoptosis of these hair cell types. CONCLUSION: These data suggest that alterations in levels of caspases and IAPs regulate hair follicle homeostasis. Moreover, finasteride appears to influence caspase and XIAP expression in hair follicle cells thus signaling anagen, active growth in the hair cycle.     

Cystatin A suppresses ultraviolet B-induced apoptosis of keratinocytes

BACKGROUND: Cystatin A is a cysteine proteinase inhibitor abundantly expressed in keratinocytes. Although cystatin A is one of the cornified cell envelope constituents and expressed in the upper epidermis, its precise function is still unknown. Ultraviolet B irradiation (UVB) induces apoptosis accompanied with the activation of cysteine proteinases, caspases. OBJECTIVE: We investigated the effect of cystatin A on UVB-induced apoptosis of keratinocytes. METHODS: We assessed the caspase activities and apoptotic cell numbers induced by UVB ittadiation in cystatin A gene transfected keratinocytes. RESULTS: UVB-induced pro-caspase 3 cleavage and caspase 3 activation were suppressed in cystatin A expression vector-transfected SV40-transformed human keratinocytes (SVHK). Furthermore, the transfected SVHK cells were resistant to UVB-induced apoptosis. In contrast neither caspase 8 nor caspase 9 activities were affected by UVB irradiation in cystatin A-transfected SVHK cells. The effects were also observed in cystatin A expression adenovirus vector-transfected cultured normal human keratinocytes (NHK). Conversely knockdown of cystatin A by si-RNA induced marked apoptosis of NHK cells following UVB irradiation accompanied with increased caspase 3 activity. In order to confirm the antiapoptotic effect of cystatin A in vivo UVB irradiation was performed on cystatin A transgenic mice (cystatin A-tg). The epidermis from cystatin A-tg was resistant to UVB-induced apoptosis compared to control mice epidermis. CONCLUSION: These results indicate that cystatin A suppresses UVB-induced apoptosis of keratinocytes by the inhibition of caspase 3 activation.     

Increased monoamine oxidase A activity in the epidermis of patients with vitiligo

Human keratinocytes under in vitro conditions synthesize norepinephrine and epinephrine, whereas melanocytes lack this capacity. Keratinocytes established from lesional and nonlesional skin of patients with vitiligo synthesized four and two times more norepinephrine, respectively, than controls. Epinephrine synthesis was similar in keratinocytes from uninvolved epidermis and controls, but cells from involved skin had 6.5-fold less epinephrine than controls, indicative of low phenylehtanolamine-N-methyl transferase (PNMT) activity. Similar results were obtained in five patients with vitiligo who showed low epinephrine levels in involved epidermis. Both human keratinocytes and melanocytes expressed significant levels of monoamine oxidase A (MAO-A) activities as shown using¹⁴C-labelled 5-hydroxytryptamine as substrate and immunohistochemical staining with mouse monoclonal antibody. MAO-A activities in the total epidermis of patients with vitiligo were increased five- to ten-fold compared with skin of type-matched controls. Similar increases in MAO-A activities were also found in both keratinocytes and melanocytes established in vitro from vitiliginous epidermis. Based on these results, it can be concluded that defective catecholamine synthesis in the epidermis of patients with vitiligo leads to increased levels of norepinephrine with a concomitant increase in MAO-A activity.     

Increased monoamine oxidase A activity in the epidermis of patients with vitiligo

Human keratinocytes under in vitro conditions synthesize norepinephrine and epinephrine, whereas melanocytes lack this capacity. Keratinocytes established from lesional and nonlesional skin of patients with vitiligo synthesized four and two times more norepinephrine, respectively, than controls. Epinephrine synthesis was similar in keratinocytes from uninvolved epidermis and controls, but cells from involved skin had 6.5-fold less epinephrine than controls, indicative of low phenylehtanolamine-N-methyl transferase (PNMT) activity. Similar results were obtained in five patients with vitiligo who showed low epinephrine levels in involved epidermis. Both human keratinocytes and melanocytes expressed significant levels of monoamine oxidase A (MAO-A) activities as shown using¹⁴C-labelled 5-hydroxytryptamine as substrate and immunohistochemical staining with mouse monoclonal antibody. MAO-A activities in the total epidermis of patients with vitiligo were increased five- to ten-fold compared with skin of type-matched controls. Similar increases in MAO-A activities were also found in both keratinocytes and melanocytes established in vitro from vitiliginous epidermis. Based on these results, it can be concluded that defective catecholamine synthesis in the epidermis of patients with vitiligo leads to increased levels of norepinephrine with a concomitant increase in MAO-A activity.     

A case of extramammary Paget's disease with depigmented macules as the sole manifestation

Summary We report a 76-year-old man who had four depigmented macules in the genital area as the sole manifestation of extramammary Paget's disease (EMP). Histologically, many scattered, dissociated, plump Paget cells, and small intraepidermal nests of these cells were seen in all four lesions. The distribution of Paget cells extended beyond the margin of the depigmented areas into adjacent normally pigmented skin. Fontana–Masson staining revealed a reduction in, or absence of, melanin deposition along the basal layer of the depigmented lesions, in contrast with an abundance of melanin along the basal layer of the adjacent normal skin. Pigment-blockade melanocytes and melanophages were seen within or below the affected epidermis. The depigmentation in this case could have been caused by a symbiotic disorder between melanocytes and keratinocytes (including melanocyte destruction), and by a disorder in melanosome transmission to the keratinocytes. This case illustrates that a depigmented macule may be a diagnostic feature of EMP. Moreover, depigmentation is probably one of the earliest clinical features of EMP, and not a neighbouring secondary change such as occurs in the Sutton's halo naevus phenomenon.     

Quantitative analysis of UVB-induced apoptosis in human epidermis

The quantitative measurement of the induction of apoptosis in cells grown in vitro can be accomplished using a variety of proven methods. However, the quantitative assay of apoptosis within an intact tissue is very laborious and the results can be misleading. We have established a method to quantitatively analyze the induction of apoptosis in human epidermis following UVB irradiation. The assay is based on the activation of the apoptotically induced enzyme caspase 3, using a synthetic caspase 3 substrate. The activation of caspase 3 was shown to correlate with the induction of apoptosis in human keratinocytes cultures as a monolayer. We then demonstrated that the activation of caspase 3 could be measured from UVB-irradiated whole skin. The induction of apoptosis was confirmed by cellular morphology and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling. Therefore, we concluded that the measurement of caspase 3 specific activity in UVB-irradiated human epidermis was an efficient, inexpensive, and accurate method to quantitate UVB-induced apoptosis in vivo.     

白癜风负压吸疱自体表皮移植的影响因素

负压吸疱自体表皮移植是目前广泛使用的稳定期白癜风治疗方法之一,具有成功率高,并发症少的优点,其疗效受多种因素影响.主要包括:负压吸疱条件如吸疱部位、温度、压力、吸疱时间等;受皮区的磨削技术;术中、术后汴意事项;术前或术后选择联合的不同治疗方法.这些因素之间亦相互作用,影响皮片内黑素细胞的含量和成活率,进而影响皮肤移植区着色程度和色素扩展范围.     

蕈样肉芽肿合并白癜风2例报告

目的：探讨蕈样肉芽肿（MF）合并白癜风的机制。方法：对2例MF色素脱失处和色素正常处皮肤活检，进行HE和Fontans染色，检查黑素细胞的分布情况。结果：2例患者的皮肤色素脱失处基底层均未见黑素颗粒，符合白癜风的病理改变；色素正常处皮肤的表皮基底层有较多黑素颗粒存在，真皮上部有黑素颗粒滴落和散在噬黑素细胞。2例患者色素脱失与色素正常处真皮内淋巴细胞浸润和分布情况不一致。结论：MF患者皮肤黑素细胞的缺失可能与其被淋巴细胞的破坏有关，而物理治疗可能促进了这种变化。     

TRAIL-induced keratinocyte differentiation requires caspase activation and p63 expression

Cornification, the terminal differentiation of keratinocytes, is a special form of programmed cell death in the skin. In this article, we report that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce the expression of the keratinocyte differentiation markers involucrin and type 1 transglutaminase in normal human epidermal keratinocytes. The induction of differentiation occurs mainly under the activation of caspases 3 and 8, and apoptosis can also be triggered. Inhibition of these apoptotic caspases attenuates both apoptosis and differentiation of keratinocytes caused by TRAIL but barely affects the induction of differentiation caused by calcium and phorbol 12-myristate 13-acetate. Differential regulation of extracellular signal-regulated kinase and p38 activation by TRAIL is also observed. Moreover, the degradation of p63 is induced by TRAIL-elicited caspase activation. However, the existence of p63 is essential for the initiation of keratinocyte differentiation by TRAIL because knockdown of ΔNp63 decreases TRAIL-induced differentiation. Taken together, our results suggest that TRAIL can be an inducer of both differentiation and apoptosis in human keratinocytes, and that caspases critically mediate these processes. This study identifies a new role of apoptotic caspases for terminal differentiation of keratinocytes and further elucidates the molecular pathways involved in this unique model of cell death.     

Alteration of the expression of Bcl-2, Bcl-x,Bax, Fas,and Fas ligand in the involved skin of psoriasis vulgaris following topical anthralin therapy

Anthralin (dithranol) is frequently used for the treatment of psoriasis. However, the mode of action of anthralin has not been completely elucidated as yet. Recent findings suggest that psoriatic keratinocytes are resistant to the apoptotic process. In this study, we examined the immunohistochemical expression of apoptosis-regulated protein in the involved psoriatic skin following topical anthralin therapy. Biopsy specimens were obtained from back skins treated with topical anthralin or white petrolatum (control) in 4 patients with psoriasis vulgaris. Immunohistochemical examination revealed that psoriatic keratinocytes expressed high levels of Bcl-x, which was significantly reduced after anthralin treatment. Bax was not detected in the epidermal keratinocytes in the petrolatum-treated skin, while it was present in the upper keratinocytes after anthralin therapy. Bcl-2 was detected only in basal layers of psoriatic epidermis following both petrolatum and anthralin application. Psoriatic keratinocytes expressed higher levels of Fas in the lower epidermis, while only weak expression was detected in anthralin-treated plaques. On the other hand, hyperproliferative keratinocytes strongly expressed Fas ligand (FasL) on their plasma membranes as well as infiltrating lymphocytes in the upper dermis. Furthermore, anthralin-treated psoriatic epidermis did not express FasL. In normal skin, keratinocytes expressed low to absent levels of Bcl-x and Bax, while Bcl-2 was detected only in melanocytes in basal layers. Neither Fas nor FasL were detected in the epidermis of normal skin. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed positive labeling on the majority of psoriatic keratinocytes through the epidermis in petrolatum-treated skin, whereas anthralin treatment markedly reduced TUNEL-positive keratinocytes. These in vivo results may reflect improvement of the psoriatic skin following effective anthralin therapy.