持久性发疹性斑状毛细血管扩张症一例

患者,男,51岁。躯干、双上肢皮疹3年余。皮肤科检查:前胸、后背及双上肢伸侧多发黄豆至甲盖大红斑,Darier征阳性。皮损组织病理检查:真皮浅层毛细血管周围稀疏单一核细胞浸润。甲苯胺蓝染色:真皮内毛细血管周围散在染色阳性细胞。诊断:持久性发疹性斑状毛细血管扩张症。     

先天性角化不良1例

患者男,21岁,具有临床三联征:全身皮肤网状色素沉着,甲营养不良和口腔黏膜白斑。并发头发稀少、干枯,有龋齿。腕部皮肤色素沉着区皮损活检示:角化过度、角化不全,基底细胞液化变性,真皮上层较多嗜色素细胞。     

持久性发疹性斑状毛细血管扩张1例

患者女,66岁。躯干、四肢泛发暗红色毛细血管扩张性斑疹1年余。Darier征阴性。皮损组织病理检查示:真皮浅层毛细血管扩张,Giemsa染色血管周围可见少数肥大细胞浸润。诊断:持久性发疹性斑状毛细血管扩张。     

大疱性色素性荨麻疹1例

患儿女,4个半月。全身色素斑4个月,起水疱10天。查体:全身弥漫性灰褐色色素斑,表面见较多水疱、大疱及糜烂结痂,尼氏征阴性,Darier征阳性。皮损组织病理检查显示真皮浅层及血管周围见较多单一核细胞浸润,G iem sa染色阳性。诊断为大疱性色素性荨麻疹。     

持久性发疹性斑状毛细血管扩张症1例

患者男,24岁,躯干及四肢褐色斑疹20余年,Darier征阳性。皮损组织病理检查示:表皮大致正常,真皮浅层毛细血管扩张,周围有单个核细胞浸润;甲苯胺蓝染色:毛细血管周围单一核细胞内有紫红色异染颗粒。诊断:持久性发疹性斑状毛细血管扩张症。     

持久性发疹性斑状毛细血管扩张症伴色素性荨麻疹1例

目的:报告1例持久性发疹性斑状毛细血管扩张症伴色素性荨麻疹。患者男,48岁。颈、躯干及四肢出现丘疹、斑丘疹4年余。皮肤科检查:颈、前胸及四肢可见红褐色丘疹、斑丘疹,间杂散在毛细血管扩张;背部可见褐色丘疹,摩擦后出现风团(Diarer征阳性)。皮损组织病理:表皮大致正常,真皮浅层毛细血管扩张,有单一核细胞浸润;Giemsa染色:真皮浅层肥大细胞浸润。诊断为持久性发疹性斑状毛细血管扩张症伴色素性荨麻疹。     

落叶性天疱疮和银屑病并发

作者报导一34岁朝鲜妇女,躯干部有瘙痒性斑疹。就诊前两周发现腰部皮损,逐渐发展至腹部,一周后,双上臂出现白色鳞屑性丘疹。查体:腰、腹、四肢有稀疏的蚕豆大小的红斑性湿疹样斑疹,几个水疱和白色鳞屑性丘疹,水疱的尼氏征阳性,白色鳞屑性丘疹有点状出血现象。病理:腰部湿疹样斑疹可见表皮内上部大疱,内含一些棘层松解细胞,真皮血管周围淋巴样细胞浸润。鳞屑性丘疹和同形反应处皮损则显示角化不全,颗粒层缺乏,粒细胞外渗至表皮,也可见到真皮乳头伸长和水肿,真皮血管扩张和淋巴样细胞浸润。直接免疫荧光检查,湿疹样斑疹的周围皮肤表     

多发性肥大细胞痣1例

报告1例多发性肥大细胞痣,患儿8月大,面额、后枕和背部多个棕灰色斑块和结节,病理检查真皮见弥漫大量肥大细胞,Darier征阳性,Gimsa染色阳性,诊断明确,有自愈可能。     

多发性肥大细胞痣1例

报告1例多发性肥大细胞痣,患儿8月大,面额、后枕和背部多个棕灰色斑块和结节,病理检查真皮见弥漫大量肥大细胞,Darier征阳性,Gimsa染色阳性,诊断明确,有自愈可能。     

HPV疫苗引起的多形红斑1例国内首报

患者女,32岁,全身出现红斑、斑丘疹、水疱伴瘙痒10 d。皮肤科情况:躯干、四肢泛发粟粒至蚕豆大孤立或融合隆起性红斑、斑丘疹,部分红斑中央可见水疱,疱壁紧张,尼氏征(-),呈典型靶形损害特点。皮损组织病理示:表皮可见浆痂,表皮内水疱形成,表皮中可见坏死的角质形成细胞,上皮脚延长,基底层液化不明显,真皮乳头水肿,真皮浅深层血管及附属器周围均可见淋巴细胞浸润,伴散在嗜酸性粒细胞浸润。诊断:多形红斑。     

他克莫司对HaCaT细胞干细胞因子mRNA及小鼠B16黑素瘤细胞c-kit mRNA表达的影响

目的 探讨他克莫司对角质形成细胞干细胞因子（SCF）mRNA及黑素细胞c-kit mRNA表达水平的影响。方法 分别培养人永生化角质形成细胞（HaCaT）和小鼠B16黑素瘤细胞,经他克莫司作用48 h后,采用实时荧光定量PCR法检测SCF mRNA及c-kit mRNA的表达。结果 他克莫司作用后,HaCaT细胞SCF mRNA、B16黑素瘤细胞c-kit mRNA的相对表达量均升高,与空白对照组比较,差异均有统计学意义（P均 ＜ 0.05）。结论 他克莫司可以上调HaCaT细胞SCF mRNA及B16黑素瘤细胞c-kit mRNA的表达量。     

Mixed skin cell lymphocyte culture reaction (MSLR) in psoriasis

The Mixed Skin Cell Lymphocyte Culture Reaction (MSLR) was studied as an in vitro approach of lympho-epidermal interactions in psoriasis. The ability of peripheral blood lymphocytes from patients with psoriasis to proliferate in response to stimulation by epidermal cells and the capacity of psoriatic epidermal cells to stimulate T cells were investigated and compared to results with cells from controls. While stimulation of control lymphocytes by autologous epidermal cells was observed, although weaker than the proliferation in response to allogeneic control epidermal cells, no stimulation was observed in autologous MSLR using psoriatic cells. The ability of epidermal cells from psoriatic skin, either uninvolved or involved skin, to induce proliferation of control lymphocytes in allogeneic MSLR did not differ from that of control epidermal cells. In contrast with results obtained with control lymphocytes and epidermal cells in allogeneic MSLR, peripheral blood cells from psoriatic subjects failed to react to stimulation by control allogeneic epidermal cells. These results indicate a normal capacity of psoriatic epidermal cells to stimulate in MSLR and a functional inability of peripheral blood lymphocytes from patients with psoriasis to react in MSLR which is in agreement with previous reports of abnormal T cell functions in the disease.     

未定类细胞组织细胞增生症一例并文献复习

报道1例未定类细胞组织细胞增生症并对既往文献进行复习。患者,女,75岁。全身丘疹、结节50天。组织病理检查:表皮萎缩变平,真皮中上层组织细胞、淋巴细胞为主间有少许泡沫细胞和多核巨细胞浸润。免疫组化:组织样细胞CD43、CD68阳性,大部分细胞CD1a阳性,部分细胞S100阳性,部分细胞CD163阳性,Ki67约30%阳性,Langerin阴性。诊断:未定类细胞组织细胞增生症。患者自行服用中草药治疗,具体不详,8个月后电话随访,皮损较前变小。     

Interleukin-10-treated dendritic cells modulate immune responses of naive and sensitized T cells in vivo

Interleukin-10 is a pleiotropic cytokine known to have inhibitory effects on the accessory functions of dendritic cells. In vitro, interleukin-10 converts immature dendritic cells into tolerizing antigen- presenting cells. To assess whether interleukin-10-treated dendritic cells exert tolerizing effects in vivo, CD4+ T cells from DO11.10 ovalbumin-T cell receptor transgenic mice were transferred to syngeneic BALB/c recipients. Recipient animals were treated with ovalbumin-pulsed/unpulsed, interleukin-10-treated/untreated CD11c+ dendritic cells thereafter and ovalbumin-specific proliferation of lymph node cells was assessed by restimulation with the peptide in vitro. In prophylactic experiments, recipients received naive CD4+ DO11.10 T cells and were immunized with ovalbumin323-339 peptide in incomplete Freund's adjuvant after treatment with various subtypes of dendritic cells. Strong ovalbumin-specific proliferation was observed in animals immunized with control ovalbumin-dendritic cells. Minimal proliferation was found in mice treated with ovalbumin-pulsed, interleukin-10-treated dendritic cells. In therapeutic experiments, preactivated CD4+ DO11.10 T cells were transferred, and recipients were treated with dendritic cells as described. Ovalbumin-specific proliferation was strong in recipients treated with ovalbumin-dendritic cells. CD4+ T cell proliferation from ovalbumin-interleukin-10-dendritic cell treated animals was below background. When delayed type hypersensitivity reactions in the footpads of prophylactically or therapeutically vaccinated animals were tested, mice treated with ovalbumin-interleukin-10-dendritic cells showed no footpad swelling compared with controls. Rechallenge with the antigen in vitro and in vivo did not alter the inhibitory effect of interleukin-10-treated dendritic cells. Thus, interleukin-10-treated dendritic cells inhibit ovalbumin-specific immune responses in naive and sensitized mice.     

Increased circulating skin-homing cutaneous lymphocyte-associated antigen (CLA)+ type 2 cytokine-producing cells, and decreased CLA+ type 1 cytokine-producing cells in atopic dermatitis

BACKGROUND: Skin-homing T cells are characterized by expression of cutaneous lymphocyte-associated antigen (CLA). Few data are available on the frequency of circulating CLA+ cytokine-producing T cells in atopic dermatitis (AD) patients. OBJECTIVES: We aimed to investigate cytokine synthesis capability vs. CLA expression in phorbol myristate acetate and ionomycin-stimulated, secretion-inhibited peripheral blood T cells of AD patients compared with healthy subjects and psoriatic patients. METHODS: Multiparameter flow cytometry was used. RESULTS: The expression of CLA among CD4+ T cells was significantly elevated in AD patients compared with healthy subjects and psoriatic patients, whereas there was no significant difference between each group in CLA expression among CD8+ T cells. The frequency of interleukin (IL)-4- and IL-13-producing cells in AD patients was significantly higher than in healthy subjects (in both CD4+ and CD8+ T-cell subsets) and psoriatic patients (in CD4+ T cells). In contrast, the frequency of interferon (IFN)-gamma-producing cells was significantly reduced in AD patients, among both CD4+ and CD8+ T cells, compared with healthy subjects and psoriatic patients. Moreover, in AD patients, the frequency of IL-4- and IL-13-producing cells was remarkably increased among the CLA+ subset (in both CD4+ and CD8+ T cells), whereas the frequency of IFN-gamma-producing cells was decreased in the CLA+ subset (in CD4+, but not in CD8+ T cells). CONCLUSIONS: These results provide evidence for the expansion of skin-homing type 2 cytokine-secreting T cells, associated with a reduction in skin-homing type 1 cytokine-producing T cells, in peripheral blood of AD patients.     

咪喹莫特对皮肤鳞状细胞癌SCL-1细胞株增生及凋亡的影响

目的 探讨咪喹莫特对体外培养人皮肤鳞状细胞癌SCL-1细胞株的增生抑制及凋亡诱导作用.方法 采用MTT法分析咪喹莫特对人皮肤鳞状细胞癌SCL-1细胞的增生,倒置显微镜观察细胞形态学,AnnexinV/PI双染流式细胞仪检测细胞凋亡,吖啶橙荧光染色检测细胞凋亡晚期形态改变,细胞死亡检测试剂盒检测细胞凋亡的程度,细胞免疫组化和RT-PCR检测凋亡相关基因Fas、bcl-2的表达.结果 咪喹莫特可明显抑制人皮肤鳞状细胞癌SCL-1细胞的增殖,并可导致其形态学改变.经0.150mg/mL咪喹莫特作用后24h,SCL-1细胞早期凋亡率最大,达47.23%;作用48h,可见典型凋亡小体.SCL-1细胞凋亡程度随咪喹莫特浓度增高、作用时间延长呈递增关系,经咪喹莫特作用后可上调Fas和下调bcl-2基因表达.结论 咪喹莫特可明显抑制SCL-1肿瘤细胞生长,诱导细胞凋亡.     

Responses of B16 melanoma cell lines, F1 and F10, to hyperthermia, lymphokine-activated killer cells and a combination of both in vitro

The cytolytic and/or cytostatic effects of hyperthermia, lymphokine-activated killer cells (LAK cells) and the combination of both were assayed using F1 and F10 B16 melanoma cell lines. F10 cells with a high metastatic potential showed a greater sensitivity to hyperthermia than F1 cells which have low metastatic potential. The F10 cells were lysed to a lesser extent by LAK cells than the F1-B16 cells. When the cell lines were subjected to hyperthermia at 43 degrees C for 3 h and then interacted with LAK cells, the maximum cytolysis reached almost 100%. When the interaction with LAK cells was followed by hyperthermia at 43 degrees C, the total release of 51Cr from the cell lines was 75-85%. The extent of 51Cr release from the B16 melanoma cell lines was inversely correlated with the survival rate as calculated by the plating efficiency of the incubated cells. The survival rate of mice intravenously injected with B16-F10 cells and subjected to hyperthermia at 41 degrees C for 3 h in vitro increased compared to that of controls. This was further increased by the simultaneous administration of LAK cells.     

VEGF促进人黑素瘤SK-MEL-1细胞侵袭性的自分泌机制初探

目的探讨血管内皮生长因子(VEGF)对人黑素瘤细胞SK-MEL-1侵袭力以及对该细胞中基质金属蛋白酶9(MMP-9)的影响,初步研究VEGF对肿瘤侵袭能力的影响及可能的作用机制。方法使用VEGF体外培养人黑素瘤SK-MEL-1细胞,免疫组化法检测该细胞VEGFR-1水平;通过细胞体外侵袭实验检测细胞侵袭能力的改变,再分别使用含20,40,80μg/LVEGF培养液培养SK-MEL-1细胞,以正常培养SK-MEL-1细胞为空白对照组,使用半定量RT-PCR和Western blot法对4组细胞中MMP-9 mRNA表达和蛋白水平进行分析。结果 VEGFR-1在SKM-EL-1细胞胞核和胞浆中均有表达。外加VEGF培养后,细胞侵袭力明显增强(P<0.01);MMP-9mRNA表达和蛋白水平在外加VEGF组明显高于空白对照组,且高浓度和低浓度组之间差异有统计学意义(P均<0.05)。结论人黑素瘤SK-MEL-1细胞系中存在有自分泌机制,VEGF可通过自分泌机制上调人黑素瘤SK-MEL-1细胞MMP-9mRNA表达及蛋白水平,进而促进肿瘤的侵袭转移。     

血管内皮生长因子-阿柔比星脂质体靶向杀伤恶性黑素瘤细胞的实验观察

目的 应用包裹阿柔比星的血管内皮生长因子（VEGF）的长循环脂质体（阿柔比星-VEGF-SSL）于体外靶向杀伤恶性黑素瘤细胞。方法 通过体外结合试验，验证阿柔比星-VEGF-SSL对恶性黑素瘤A375细胞的特异结合能力。通过体外细胞毒试验（MTT），检测阿柔比星-VEGF-SSL对A375细胞增殖活性的影响。结果 阿柔比星-VEGF-SSL可与A375细胞特异结合，结合率可达非特异性脂质体的2.15倍。阿柔比星-VEGF-SSL可特异抑制A375细胞的增殖活性。48 h细胞毒试验阿柔比星-VEGF-SSL抑制A375细胞增殖活性的作用与游离阿柔比星相似（P ＞ 0.05），优于无VEGF的阿柔比星脂质体（阿柔比星-SSL）（P ＜ 0.05），而对非靶细胞（黑素细胞）增殖活性的抑制作用弱于两者。0.5 h预处理试验表明：缩短药物与细胞接触时间后，阿柔比星-VEGF-SSL仍保持较强抑制A375细胞增殖活性的作用。结论 阿柔比星-VEGF-SSL可特异性识别恶性黑素瘤A375细胞，并作为良好载体将阿柔比星带入瘤细胞，显著抑制A375细胞的增殖活性，实现其靶向杀伤作用。     

吲哚胺2,3-双加氧酶在尖锐湿疣皮损中表达的研究

目的 分析尖锐湿疣组织中吲哚胺2,3-双加氧酶(IDO)水平,研究其局部代谢色氨酸的能力.方法 免疫组化法观察尖锐湿疣患者皮肤IDO蛋白表达情况,计数IDO阳性细胞的比例.免疫荧光观察IDO(+)细胞与树突细胞的关系.分离对照皮肤角质形成细胞和疣体上皮细胞,色氨酸体外孵育后检测上清液中色氨酸代谢产物犬尿氨酸的浓度以反映细胞代谢色氨酸的能力.结果IDO(+)细胞在正常皮肤中非常少,但在疣体表皮中却大量聚集.疣体内IDO(+)细胞/总体细胞48.3%±15.4%显著高于正常皮肤5.2%±2.4%,差异有统计学意义(P<0.05).IDO(+)细胞的荧光信号和皮肤朗格汉斯细胞并不重合,提示来源于疣体表皮细胞.从疣体组织分离的上皮细胞在体外代谢色氨酸的能力强于健康对照皮肤中分离的表皮细胞.结论 尖锐湿疣疣体中存在大量的IDO(+)细胞,这些细胞可能参与尖锐湿疣的发病.