白癜风患者表皮内郎格罕细胞观察

用改良的Ｊｕｈｌｉｎ－ＳｈｅｌｌｅｙＡＴＰ酶细胞化学染色法检查了１３例白癜风（进展期）患者的白斑、白斑边缘区及对侧相应正常皮肤中郎格罕细胞情况，结果白斑部位表皮郎格罕细胞数目较对应正常皮肤表皮变化不大，而白斑边缘部皮肤郎格罕细胞数目较正常皮肤显著增多（Ｐ＜０．００５）。在白斑及白斑边缘区还可见到印格罕细胞的形态学变化：胞体变大、深染、胞突消失以及细胞积聚现象，在白斑边缘部尤其明显。本研究显示郎格罕细胞数目和形态学的变化与病情活动有关。提示郎格罕细胞在白癜风发病机制中起一定的作用。     

Preliminary evaluation of vitiligo using in vivo reflectance confocal microscopy

BACKGROUND: Vitiligo is the most common pigmentary disorder with a global incidence from 0.1% to 2% in different geographical areas. Histopathology and histochemistry have shown the reduction of melanocytes in achromic patches, but microscopic changes of lesional and non-lesional skin are still not completely understood. Reflectance confocal microscopy (RCM), based on the different light reflectance index of cutaneous structures, allowed in vivo, en face microscopic evaluation of superficial skin layers with a resolution similar to skin histology. AIM: The purpose of this study was to evaluate RCM features of lesional and non-lesional skin of vitiligo patients. Moreover, re-pigmented areas were taken into consideration in order to evaluate melanocyte response to ultraviolet B (UVB) radiation. SUBJECTS AND METHODS: Sixteen patients of different phototypes affected by active non-segmental vitiligo and 10 controls were enrolled in the study. In vivo skin imaging was done using a commercially available RCM (Lucid, Vivascope 1500. Re-pigmented areas from 6 to 16 patients (after UVB narrow-band therapy) were also examined. RESULTS: Vitiligo lesions showed the disappearance of the bright rings normally seen at the dermo-epidermal junction. Moreover, non-lesional skin of vitiligo patients showed unexpected changes as the presence of half-rings or scalloped border-like features of the bright papillary rings. In re-pigmented areas after UVB narrow band therapy, the presence of activated, dendritic melanocytes was seen. CONCLUSIONS: Considering our results, and following further studies, RCM clinical applications could be used in the therapeutic monitoring and evaluation of the evolution of vitiligo.     

Fc epsilon R11/CD23 receptor distribution in patch test reactions to aeroallergens in atopic dermatitis.

There is increasing evidence that exposure to organic allergens may induce or exacerbate lesional skin in patients with atopic dermatitis. In this study, patients with atopic dermatitis were patch tested to 11 common organic allergens and to control chambers containing 0.4% phenol and 50% glycerin in 0.9% saline. In biopsies from positive patch test reactions, patch test control skin, lesional eczematous and non-lesional skin from atopic individuals, and normal skin from non-atopic volunteers, the presence and distribution of macrophages (RFD7+), dendritic cells (RFD1+), and Langerhans cells, and the expression of the low-affinity receptor for IgE (CD23) were investigated. In patch test reactions and lesional skin samples, inflammatory infiltrates of diffusely distributed macrophages (RFD7+), dendritic cells (RFD1+), T lymphocytes (RFTmix+), and Langerhans cells (CD1+) were seen, the latter being present in both the epidermis and the dermis. The numbers of Langerhans cells were reduced in the epidermis and increased in the dermis in patch test reactions and lesional skin compared to their controls. Double staining revealed a change in the distribution of CD23 antigen. In patch test control and non-lesional biopsies many macrophages and only a few Langerhans cells within the dermal infiltrates expressed this antigen. In patch test reaction and lesional skin samples, however, the proportion of CD23+ dermal Langerhans cells had increased compared to macrophages. Furthermore, in these latter samples an increased proportion of dermal CD1+ cells expressed the dendritic cell (RFD1+) marker. These results show that following antigen challenge there are marked similarities between the phenotype of the cellular infiltrate in patch test reaction and lesional skin biopsies, and also demonstrate a changing distribution of CD23 on antigen-presenting cells.     

Aberrant expression of complement regulatory proteins, membrane cofactor protein and decay accelerating factor, in the involved epidermis of patients with vitiligo

BACKGROUND: Vitiligo is a pigmentary disorder of the skin characterized by the complete absence of melanocytes from the lesion. Complement-activating antimelanocyte antibodies have been implicated in vitiligo pathogenesis. As membrane regulators of complement activation, membrane cofactor protein, decay accelerating factor and CD59 protect cells from elimination by autologous complement, their absence or downregulation on melanocytes may be associated with autoantibody and complement-mediated melanocyte destruction in vitiligo. OBJECTIVES: We studied the expression of these regulatory proteins in non-lesional, perilesional and lesional vitiligo skin compared with those of control specimens. METHODS: We used immunohistochemistry to study the expression of the regulatory proteins, and flow cytometric analysis of cultured melanocytes to investigate possible constitutive changes in the expression levels of these molecules. We also investigated whether melanocytes can influence keratinocyte susceptibility to autologous complement by regulating keratinocytic decay accelerating factor and membrane cofactor protein expression levels. RESULTS: Immunohistochemical data showed that expression of membrane cofactor protein and decay accelerating factor in whole epidermis was lower in lesional and perilesional skin in comparison with non-lesional skin. The reduced in situ expression appeared to be specific to vitiligo. However, coculture experiments indicated that melanocytes do not influence keratinocyte susceptibility to autologous complement. Further, flow cytometric analysis of cultured melanocytes convincingly demonstrated that non-lesional vitiligo and control melanocytes have comparable decay accelerating factor, membrane cofactor protein and CD59 expression levels. CONCLUSIONS: It is therefore concluded that there is no constitutive melanocyte defect per se that could be related to the in vivo expression of these molecules in vitiligo. Nevertheless, the present data suggest that both keratinocytes and melanocytes in the involved vitiliginous whole epidermis express lower levels of decay accelerating factor and membrane cofactor protein compared with controls that could render them more vulnerable to autologous complement attack.     

系统性红斑狼疮患者CD1a、CD68、HLA-DR等的研究

目的 研究系统性红斑狼疮(SLE)患者外观正常及病变皮肤中朗格汉斯细胞(LC)一些重要表面标志的变化。方法 应用CD1a、CD68和HLA-DR等单克隆抗体和ABC免疫组化技术对9例SLE患者外观正常和皮损部位的组织进行了免疫表型检测。结果 ①SLE皮损中LC的数量减少,且其形态与表面标志亦有变化;②SLE病损处的角质形成细胞(KC)强弱不等地表达HLA-DR抗原,个别病例的外观正常皮肤KC也可局灶性表达HLA-DR抗原;③SLE外观正常皮肤或皮损的表皮中均未见细胞间粘附分子1和CD4阳性LC,仅在真皮的浸润细胞中见到较多的阳性细胞;④发现在SLE外观正常皮肤和皮损表皮内出现两类CD68阳性的树枝状细胞;在SLE皮损的浸润细胞中CD68阳性树枝状细胞大量增加;⑤细纤维状CD68阳性物质呈网状围绕基底部的KC,这些细纤维状阳性物质有些与表皮树枝状细胞相连,有些则没有明显的关系。结论 SLE外观正常和病变皮肤中LC一些重要表面标志的变化有所不同。外观正常皮肤和皮损表皮内出现两类树枝状细胞,一类可能为LC,而另一类则来源不清;在SLE皮损的浸润细胞中这些CD68阳性树枝状细胞大量增加,表皮内存在CD68阳性纤维状染色,其意义尚需进一步研究。     

Abnormal nuclear expression of aquaporin-3 in lesional and perilesional skin of vitiligo patients: A novel immunohistochemical finding

Background

Vitiligo is a skin disease characterized by a complex etiopathogenesis. Keratinocyte apoptosis may play a role in vitiligo pathogenesis. Aquaporin-3 (AQP-3) is an aqua-glyceroporin that controls keratinocyte proliferation and differentiation.

Aim

To assess the immunohistochemical expression of AQP-3 in lesional and perilesional skin of vitiligo patients compared to healthy control skin.

Methods

A total of 20 patients with generalized non-segmental vitiligo and 20 age- and sex-matched healthy controls were included. Lesional and perilesional skin of vitiligo patients, as well as normal skin of control subjects, were biopsied. The immunohistochemical expression of AQP3 in the epidermis was examined.

Results

Compared to control skin, both lesional and perilesional skin showed a significant reduction in the intensity of membranous staining of AQP-3 (p < 0.001, p = 0.002, respectively). Moreover, the membrano-cytoplasmic pattern of AQP-3 staining was significantly detected in 80% of lesions and 85% of perilesional biopsies, while it was absent in control skin (p < 0.001). Additionally, nuclear AQP-3 expression was significantly detected in 35% of lesions and 55% of perilesional biopsies, while it was not detected in control skin (p = 0.012, p < 0.001, respectively). No statistically significant difference was detected between lesional and perilesional skin.

Conclusions

To our knowledge, this is the first immunohistochemical research to show a significant abnormal nuclear expression of AQP-3 in lesional and perilesional skin of vitiligo patients. This abnormality may reflect impaired functions of AQP-3, leading to keratinocyte apoptosis with subsequent melanocyte death and development of vitiligo.     

结合珠蛋白在银屑病皮损及皮损周边外观正常皮肤中的表达

目的 从mRNA及蛋白质水平研究结合珠蛋白在银屑病皮损及皮损周边外观正常皮肤中的表达,探讨其与朗格汉斯细胞的关系及在银屑病发病中的作用.方法采用免疫组化、免疫荧光双标记和原位杂交技术检测银屑病皮损及皮损周边外观正常皮肤中结合珠蛋白的表达.结果与正常人皮肤相比,银屑病皮损处角质形成细胞中结合珠蛋白mRNA的表达均明显增强(P＜0.001);皮损周边外观正常皮肤中的表达与正常人皮肤差异无显著性(P＞0.05).免疫组化显示:皮损处部分角质形成细胞胞浆中有结合珠蛋白表达;皮损及皮损周边外观正常皮肤中均可见结合珠蛋白在部分朗格汉斯细胞中呈阳性表达,且两者中结合珠蛋白阳性朗格汉斯细胞与朗格汉斯细胞总计数的比值较正常皮肤显著增高(P＜0.001).结论银屑病皮损处角质形成细胞中结合珠蛋白mRNA的表达增强,并能合成结合珠蛋白.合成结合珠蛋白的角质形成细胞可能在银屑病发病机理中起负反馈调节作用。     

Gene expression analysis of melanocortin system in vitiligo

BACKGROUND: The melanocortin system in the skin coordinates pigmentation and immune response and could be implicated in the pathogenesis of vitiligo. OBJECTIVES: We aimed to analyze changes in expression of genes involved in skin pigmentation (melanocortin system and enzymes involved in melanin synthesis). METHODS: With quantitative RT-PCR we measured the mRNA expression levels of eight genes from the melanocortin system and two enzymes involved in melanogenesis. RNA was extracted from both lesional and non-lesional skin of vitiligo patients and in non-sun-exposed skin of healthy subjects. RESULTS: POMC (proopiomelanocortin) expression was lower in lesional skin compared to non-lesional skin. Expression of melanocortin receptors was increased in unaffected skin of vitiligo patients compared to healthy subjects and decreased in lesional skin compared to uninvolved skin of vitiligo patients, the differences were statistically significant in the cases of MC1R (melanocortin receptor 1) and MC4R (melanocortin receptor 4). TRP1 and DCT genes were down-regulated in lesional skin compared to non-lesional vitiligo skin or skin of healthy controls and up-regulated in uninvolved vitiligo skin compared to healthy control samples. In non-lesional skin, POMC expression was not elevated, possibly indicating that systemic influences are involved in up-regulation of MC receptor genes. Decreased expression of the analyzed genes in the lesional skin is not surprising, but statistically significant increased expression of studied genes in non-lesional skin from vitiligo patients is not described previously. CONCLUSION: In our mind, up-regulation of melanocortin system in non-lesional skin could be systemic compensation to restore normal pigmentation in lesions.     

Immunopathologic characterization of the tissue response in endemic pemphigus foliaceus (fogo selvagem)

BACKGROUND: The research on endemic pemphigus foliaceus (fogo selvagem) has mainly focused on the humoral immune response, but little attention has been given to the function of cell-mediated immune response and the nature of the cellular elements of the tissue reaction in the lesions of fogo selvagem. OBJECTIVE: The purpose of this study was the immunophenotype characterization of the inflammatory cells as well as the expression of adhesion molecules and HLA-DR in the perilesional and lesional skin of fogo selvagem. METHODS: Twenty biopsy specimens of lesional and perilesional skin were analyzed by immunohistochemical techniques. The panel of monoclonal antibodies consisted of CD8, CD4, CD1a, HLA-DR, IL-2R, LFA-1, ICAM-1, and PAN-B. RESULTS: The semiquantitative analysis of the cell population revealed a predominance of CD4 T lymphocytes in the tissue response of perilesional and lesional skin. The population of epidermal Langerhans cells was decreased in lesional skin when compared with the perilesional skin, whereas CD1a(+) dermal dendritic cells predominated in lesional skin. Keratinocyte expression of ICAM-1 and HLA-DR was negative in both lesional and perilesional skin. CONCLUSION: The overall results suggest the participation of the cell-mediated immunity in endemic pemphigus foliaceus (fogo selvagem). The lack of keratinocyte ICAM-1 expression may be related to the pattern of cytokines secreted by the CD4(+) T cells of the tissue reaction in fogo selvagem.     

Increased expression of adhesion receptors in both lesional and non-lesional psoriatic skin

Adhesion receptors and their ligands play a vital role in the immune system. We studied the expression of different adhesion receptors, using single- and double-staining immunohistochemical techniques, in both lesional and non-lesional skin specimens from seven psoriasis patients and in skin biopsy specimens from eight normal healthy controls. Our results showed an overall increased expression of several adhesion receptors in both lesional and non-lesional psoriatic skin. We consistently found an increased expression in particular of ICAM-1 and E-selectin on endothelial cells, and ICAM-1 on T cells and Langerhans cells. In contrast, a weak expression of VCAM-1 was found on endothelial cells and mononuclear cells in lesional psoriatic skin specimens alone. Interestingly, LFA-1 was also expressed on Langerhans cells, with a greater frequency in skin from lesional than from non-lesional sites, but was never expressed in skin from normal healthy individuals. Furthermore, significantly increased numbers of Langerhans cells and T cells with a positive reactivity for MAb HECA-452 were found in both lesional and non-lesional psoriatic skin. We hypothesize that the enhanced expression of adhesion receptors on migrating immunocompetent cells and endothelial cells of psoriatic skin in general facilitates the increased influx of activated T lymphocytes and other immunocomponent cells into the skin, and thus underscores the generalized character of the disease.     

Over-expression of tumor necrosis factor-α in vitiligo lesions after narrow-band UVB therapy: an immunohistochemical study

There is a growing evidence that cytokines are important in the depigmentation process of vitiligo, however, the exact mechanism is not fully understood. The aim of this work was to study the possible role of the tumor necrosis factor-?? (TNF-??) cytokine in the depigmentation process of the disease. Twenty patients with generalized vitiligo were exposed to narrow-band ultraviolet B (NB-UVB) therapy thrice weekly for a total of 60 sessions. Immunohistochemical examination was done, to assess the TNF-?? expression in lesional and perilesional skin as compared to normal control skin, before and after therapy. At baseline, positive lesional TNF-?? expression was detected in 60?% of patients which was significantly higher as compared to perilesional skin (20?%) and negative expression in healthy control skin. Post-treatment, a statistically significant increase in TNF-?? expression was detected in both lesional (90?%) and perilesional skin (70?%) as compared to baseline (P?<?0.05). The significant increase of TNF-?? in vitiligo lesions compared with perilesional and healthy skin suggests a possible involvement of this cytokine in the depigmentation of vitiligo. The increase in TNF-?? expression after NB-UVB phototherapy suggests another role in repigmentation.     

干细胞因子及其受体在寻常型白癜风表皮中的表达

目的 探讨SCF/c-kit信号通路在白癜风发病中的作用。方法 采用免疫组化和RT-PCR法检测17例寻常型稳定期白癜风患者和10例正常对照标本中表皮角质形成细胞的干细胞因子表达及基底层黑素细胞c-kit的表达情况。结果 白癜风非皮损区干细胞因子、c-kit蛋白表达与正常对照无明显差异(P>0.05),皮损区干细胞因子表达显著高于正常对照皮肤(P<0.05),而c-kit表达显著低于正常对照皮肤(P<0.05)。白癜风非皮损区表皮干细胞因子、c-kit mRNA表达平均水平与正常对照近似(P>0.05);皮损区干细胞因子mRNA表达水平高于非皮损区及正常对照组差异有统计学意义(P<0.05);皮损区c-kit mRNA表达水平显著低于非皮损区及正常对照组(P<0.05)。结论 SCF/c-kit的异常表达可能与白癜风的发病有关。     

Clinical and histopathologic characteristics of trichrome vitiligo

BACKGROUND: The term trichrome vitiligo describes lesions that have a tan zone of varying width between normal and totally depigmented skin, which exhibits an intermediate hue. However, the pathogenesis and the histopathologic characteristics of trichrome vitiligo are unknown. OBJECTIVE: Our purpose was to investigate the clinical and histopathologic characteristics and the pathogenesis of trichrome vitiligo. METHODS: Four punch biopsy specimens were taken from 21 patients with trichrome vitiligo; they were from vitiliginous skin, light brown skin, perilesional normal skin, and normal skin as far as 5 cm from the nearest vitiligo spot. The sections were stained with hematoxylin-eosin; in selected cases, we performed immunohistochemical staining with S-100 protein and CD1a. RESULTS: Trichrome vitiligo occurred most frequently on the trunk in active vitiligo vulgaris. Focal vacuolar degeneration of the basal cell layer and mild inflammatory cell infiltration of the epidermis and dermis were more prominent in light brown skin and perilesional normal skin than in vitiliginous skin and normal skin. The number of melanocytes was decreased in light brown skin compared with perilesional normal skin (P <.05) and in vitiliginous skin compared with light brown skin (P <.05); a few melanocytes were observed even in skin affected by trichrome vitiligo. The number of Langerhans cells was increased in the epidermis of light brown skin and perilesional normal skin compared with vitiliginous and normal skin (P <.05). PUVA therapy yielded excellent repigmentation. CONCLUSION: Trichrome vitiligo is a variant of active vitiligo. The changes of melanocytes, keratinocytes, and Langerhans cells may be involved in the pathogenesis of depigmentation in trichrome vitiligo.     

Expression and modulation of apoptosis regulatory molecules in human melanocytes: significance in vitiligo

Although the aetiology of the hypopigmentary disorder vitiligo is ill understood, it is clear that pigment producing cells are absent from vitiliginous lesional skin. The present study was designed to investigate the possible role of melanocyte-expressed apoptosis regulatory molecules in melanocyte disappearance. Flow cytometric evaluation of p53, p21, Bcl-2 and Bax revealed no differences in in vitro expression levels between normal control and non-lesional melanocytes. Moreover, no in situ immunohistological differences were observed in melanocytes present in control, non-lesional and perilesional skin. However, an enhanced number of p53+ nuclei, in the absence of detectable p21 expression, was detected in involved areas. The observed p53 expression pattern did not involve melanocytes and could be the result of ultraviolet (UV) A irradiation. Further, we showed that UVB is capable of modulating melanocyte-expressed apoptosis regulatory molecules. Consequently, a lethal dose of UVB was given to two groups of cultured normal control and non-lesional melanocytes. No significant differences were found when comparing the percentages and kinetics of UVB-induced apoptosis in these groups. In conclusion, our results indicate that the relative apoptosis susceptibility of melanocytes in vitiligo is comparable with that of normal control cells. It is therefore unlikely that vitiligo is causally related to dysregulation of apoptosis regulatory molecules.     

采用生物信息学方法筛选和分析白癜风差异表达基因

目的:通过生物信息学方法探索与白癜风进展相关的信号通路和基因。方法:从GEO数据库中下载白癜风芯片检测数据集GSE75819,利用R语言软件中limma包的LMFit和eBayes函数筛选15例印度白癜风患者皮损与非皮损组织间的差异表达基因（DEG）。通过京都基因与基因组数据库（KEGG）、基因本体论（GO）分析和基因...     

Expressional changes in the intracellular melanogenesis pathways and their possible role in the pathogenesis of vitiligo

BACKGROUND: Main pathway in human melanocytes through which signal from the melanocortin system reaches the melanogenesis enzymes is cAMP/PKA pathway and it is modulated by Wnt and MAPK pathways. In our previous study we established significant increase of melanocortin receptor expression in unaffected skin of vitiligo patients compared to healthy subjects. OBJECTIVE: The aim of this study was to assess the gene expression profile of the intracellular signalling pathways linking melanocortin system with enzymes involved in melanogenesis. METHODS: Using QRT-PCR method, mRNA expression levels of eight genes related to signal transduction from the melanocortin system to melanogenesis enzymes was measured in lesional and non-lesional skin of vitiligo patients and in the skin of healthy control subjects. Following genes were analyzed in the study: MITF, CREB1, p38, USF1, PIK3CB (PI3K), RPS6KB1, LEF1 and BCL2. RESULTS: The mRNA levels of MITF, LEF1, p38, PIK3CB and RPS6KB1 were decreased in lesional skin of vitiligo patients compared to skin of healthy control subjects. We also found increased expression of USF1 and BCL2 in non-lesional skin of vitiligo patients compared to skin of healthy control subjects. mRNA levels of MITF and BCL2 were decreased in lesional skin of vitiligo patients compared to non-lesional skin of vitiligo patients. CONCLUSIONS: Present study indicates increased expression of the genes of the intracellular melanogenesis pathway in the non-lesional skin of vitiligo patients. This finding suggests activation of melanogenesis pathway in the non-lesional skin of vitiligo.     

尖锐湿疣患者皮损中朗格汉斯细胞和浆细胞样树突细胞的检测

目的 探讨朗格汉斯细胞（LC）和浆细胞样树突细胞（pDC）在尖锐湿疣（CA）感染发病机制中的可能作用。 方法 免疫组化SP法检测23例CA患者皮损中CD1a+LC和CD2AP+pDC、CD123+pDC的表达和分布情况,以其中13例CA组织的边缘正常皮肤为对照,比较CA皮损和边缘正常皮肤中CD1a+LC、CD2AP+pDC、CD123+pDC表达密度和阳性率的差异。 结果 CD1a+LC主要位于表皮基底层上棘层,少数在真皮乳头层。CA皮损中CD1a+LC在表皮层和真皮层的密度及阳性率与边缘正常对照组比较,差异无统计学意义（P > 0.05）。CD2AP+pDC、CD123+pDC主要位于真皮乳头层,CA患者皮损中CD2AP+pDC、CD123+pDC的密度和阳性率均比边缘正常对照组显著增高（P < 0.05）。 结论 人乳头瘤病毒感染影响局部黏膜的pDC数量,LC数量未见变化。     

Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion

The aetiology of vitiligo remains obscure. In this study, the role of integrins in the observed inability of melanocytes to repopulate lesional skin was investigated. Antibodies directed to α₂, α₃, α₅, α_v, α₆, β₁ and β₃ integrin subunits were used. Immunohistology revealed no marked differences in the overall levels of expression of integrins between control, non-lesional, perilesional or lesional skin. Moreover, no differences were noted in the level of expression of integrins or the adhesive capacity between cultured control cells derived from three separate donors and vitiligo-derived melanocytes from two donors. Rather, it was clearly observed that towards the lesion, vitiligo skin contains increasing amounts of tenascin in the basal membrane and papillary dermis in five patients employing T2H5 antihuman tenascin antibody. The anti-adhesive effect observed in vitro for this extracellular matrix molecule using normal melanocytes may contribute to loss of pigment cells in vitiligo or to ineffective repopulation of the lesions.     

Epidermal Langerhans cells in actinic prurigo: a comparison between lesional and non-lesional skin

Background  Actinic Prurigo (AP) is a chronic pruritic dermatosis of unknown cause affecting sun exposed skin in defined ethnic groups with characteristic MHC alleles. However, the cutaneous dendritic cells have not been assessed.
Objective  To assess in situ the epidermal Langerhans Cell (LC) status in Actinic Prurigo.
Study design  Fresh skin samples from three AP patients were used to evaluate in situ the epidermal LC, comparing lesional and non-lesional sites in each subject.
Setting  AP patients attending the Dermatology Department at the Hospital M. Gea-Gonzalez in Mexico city.
Methods  Lesional and non-lesional skin samples were taken from each subject to prepare both epidermal sheets and conventional tissue sections. Three markers restricted to LC in epidermis (CD1a, ATPase, MHC-II) were used to quantify the LC per area in epidermal sheets.
Results  Compared to non-lesional skin from the same subject, a significant reduction in the number of LC per area of epidermis was found in lesional skin; with any of the three markers evaluated.
Conclusion  The frequency of epidermal LC decreases importantly in lesional skin from AP patients.