郎格罕细胞是MF真皮浸润中常见的细胞成分吗?

有些作者曾提示,MF病人的真皮浸润中有郎格罕细胞(LC),这是他们基于的T6阳性细胞的存在或在超微结构中见到认为是LC的特殊细胞学标记的Birbeck颗粒.但在MF的真皮浸润中,超微结构曾见到的树突细胞与曾由Veldman描述     

斑秃皮损内朗格汉斯细胞及CD8+ T细胞的数量及分布分析

【摘要】 目的 探讨斑秃患者脱发皮损中朗格汉斯细胞在斑秃病理进程中的分布以及与T细胞的关系。 方法 对29例斑秃患者（活动期16例,非活动期13例）头皮脱发皮损进行CD1a免疫组化染色,对其中17例斑秃患者行CD4、CD8免疫组化染色。荧光半定量PCR测定局部皮损浅层和深层CD1a和粒细胞巨噬细胞刺激因子（GM-CSF）的mRNA表达水平。 结果 斑秃患者表皮和真皮各处包括真皮浅层血管周围、毛囊周围,真皮深层血管周围、毛囊周围CD1a阳性LC数量均较健康对照显著增加（Z = 4.354,2.884,4.640,3.217, 3.496,均P ＜ 0.01）,活动期皮损表皮层、深层血管、深层毛囊CD1a阳性LC数量较非活动期皮损高（Z = 2.457, 2.130,1.954,P ≤ 0.05）。斑秃患者CD1a 、GM-CSF mRNA相对表达量在皮损真皮浅层虽与健康对照无差异,但在深层均高于健康对照（Z = 2.702,2.941,均P ＜ 0.01）。斑秃患者浅层血管周围LC与深层毛囊周围CD8+ T细胞数量呈正相关（r = 0.618,P ＜ 0.05）,活动组浅层血管周围LC与深层毛囊周围CD8+ T细胞数量分布呈正相关关系（r = 0.795,P = 0.01）,非活动组浅层血管周LC与深层毛囊周围CD8+ T细胞数量分布则无相关关系。 结论 斑秃患者皮损LC数量增加,且在活动期皮损升高更明显。活动期斑秃皮损中浅层血管周围LC与深层毛囊周围CD8+ T细胞数量呈正相关,推测LC在斑秃疾病进展中发挥作用。     

传染性软疣中免疫激活细胞及上皮细胞的变化

为了解传染性软疣中郎格罕细胞(LC)、T细胞亚群、真皮树突状细胞及角朊细胞激活标记的变化以及HLA-Ⅰ及HLA-Ⅱ类抗原的表达,作者对10例传染性软疣患者的皮损进行了免疫组化研究.标本取自10例患者不同病期的典型传染性软疣损害,冰冻切片,丙酮固定后采用生物素亲和素方法染色.对照组用含5%牛血清白蛋白的PBS液代替,荧光显微镜观察结果.结果发现,所有传染性软疣病损中免疫活性细胞(T细胞及LC)完全缺乏.软疣小体中表皮生长因子(EGF)及转铁白受体强阳性,β_2-微球蛋白阴性.奇怪的是所有标本感染后的某些角朊细胞也表达了OKM5膜抗原.皮损下方的真皮中可见散在或密集的HLA-DR阳性细胞.单个核细胞浸润     

CD1a、CD68在继发性瘢痕疙瘩中的表达及意义

目的 探讨继发性瘢痕疙瘩皮损中表皮朗格汉斯细胞（LC）和真皮CD68阳性组织细胞的分布和密度。方法 取30例继发性瘢痕疙瘩患者的皮损、14例正常人皮肤组织切片进行CD1a和CD68免疫组化染色。以测微尺标定目镜方格计数方格内阳性细胞数,计算出单位面积内细胞的密度。组间比较采用SPSS软件进行 Student t检验。结果 在继发性瘢痕疙瘩表皮内CD1a阳性LC密度为（61 ± 49）个/mm2,正常表皮为（258 ± 61）个/mm2,两组比较,t = 9.88,P ＜ 0.01;继发性瘢痕疙瘩真皮CD1a阳性细胞密度为（40 ± 65）个/mm2。继发性瘢痕疙瘩表皮中无CD68阳性细胞,真皮内CD68阳性组织细胞密度为（287 ± 73）/mm2,正常皮肤为（290 ± 22）个/mm2,两组比较,t = 0.02,P ＞ 0.05。继发性瘢痕疙瘩真皮浅层CD68阳性组织细胞占真皮中所有细胞的62% ± 12%,而正常皮肤为70% ± 14%,两组比较,t = 2.66,P ＜ 0.05。 结论 继发性瘢痕疙瘩表皮中LC减少,无CD68阳性的细胞。真皮中LC增多;真皮浅层CD68阳性组织细胞占真皮中所有细胞的比例下降。     

郎格罕细胞与皮肤病

郎格罕细胞(LC)是一种树枝状细胞,不仅位于表皮层,也见于真皮及附属器、粘膜、淋巴管、淋巴结、胸腺以及毛细血管内.正常人表皮LC密度为400～1,000个/mm~2,占表皮细胞的3～8%.LC特征性的电镜标记是Birbeck颗粒,组化标记是ATP酶,免疫学标记是Ⅰa抗原和OKT_6抗原.可通过电镜、组化和免疫荧光或免疫酶法鉴定LC.     

尖锐湿疣局部细胞免疫功能状态与人乳头瘤病毒型的相关性研究

我们采用 (1)聚合酶链反应检测皮损中HPV6 11、16 18。 (2 )应用免疫组化技术对 6 1例CA患者疣体组织、疣旁“正常”组织及 2 0例对照包皮组织表皮中CD1a+ 朗格汉斯细胞 (LC)及表真皮中CD4 +T、CD8+ T细胞数目及CD4 + CD8+ 比值进行检测。探讨CA患者局部细胞免疫功能状态与HPV型的关系。结果CA疣体组织表皮CD1a+ LC细胞数量较正常对照明显降低 (P <0 .0 1) ,不同HPV亚型感染所致CA其CD1a+ LC数目差异无显著性 (P >0 .0 5 ) ;真皮中CD4 + T、CD8+ T细胞数目较正常对照升高 ,但CD4 + CD8+ 比值下降 (P <0 .0 1) ;CD4 + T、CD8+ T细胞数目及CD4 + CD8+ 比值相应的改变与不同HPV亚型无关。表皮CD1a+ LC与表皮、真皮中CD4 + T细胞及CD4 + CD8+ 比值成正相关 ,与CD8+ T细胞数目成负相关。因此 (1)CA患者皮损局部细胞免疫功能低下 ;疣体组织中CD1a+ LC细胞数目及CD4 + CD8+比值均降低。 (2 )CA患者局部免疫缺陷程度与HPV型无相关性。     

银屑病皮损中郎格罕氏细胞的初步观察

本文应用ATP酶法和抗T6单克隆抗体OKT6直接免痊荧光法,对6例寻常型银屑病皮损及其邻近正常皮中的LC进行了初步对比观察.结果两法在正常皮肤部位显示表皮内的LC带有树枝状突起,分布均匀,主要位于中层;且OKTs法尚可显示真皮内少最散在的LC.而皮损部位则表皮内LCJL平消失,偶见1~2七且其突起消失.呈小圆圈状;真皮内未见可辨认的LC.以上所见提示皮肤中的LC可能与银屑病的发病机理有关.     

异位性皮炎——细胞介导和IgE介导的免疫病理反应

异位性皮炎(AD)患者皮损及对吸入性变应原产生的湿疹样反应中,真皮的浸润细胞主要是活化的TH细胞和郎格罕细胞(LC),故认为细胞介导的免疫反应参与了AD皮损的发生.最近发现,AD患者表皮LC结合IgE分子,并认为对AD提供了特异的诊断依据.由此可见,AD可能是IgE介导和细胞介导的混合反应.     

簟样肉芽肿的T细胞亚群和郎格罕细胞的分布及对PUVA治疗的效果

作者选择23名经组织学证实为蕈样肉芽肿(MF)的病人,在PUVA治疗前后每人取4处病理标本,共55处,应用单克隆抗体技术检测T细胞亚群及郎格罕细胞(LC)的分布.计算T辅助细胞(T_H)及T抑制/细胞毒细胞(T_(sc))占淋巴样浸润细胞总数的百分数,并以T_H∶T_(sc)比率来表示结果,表皮LC以每毫米长表皮中所含的数量表示.结果发现真皮内T_H∶T_(sc)比率变化在0.6～18之间,表皮在0.15～10之间.84%病人真皮浸润细胞及55%病人表皮浸润细胞中T_H数量显著多于T_(sc),但9%     

用APAAP免疫组化方法研究CD1(OKT6)抗原在正常及SLE皮疹组织中的分布

本文以APAAP免疫组化方法及HIT6-1McAb检测了各种正常及病变组织中相应抗原的分布,所检测的正常组织包括5-6个月引产胎儿之心、肺、肾、脑、肝、平滑肌、横纹肌、甲状腺、胸腺、胃肠,成人肝、肾、扁桃体、淋巴结、骨髓等.病变组织包括ITP脾、溶血性贫血脾、再障扁桃体与食道,肺的鳞癌、腺癌及12例活动期的SLE皮疹组织.发现95以上的胸腺皮质淋巴样细胞以及扁桃体、淋巴结及脾脏中的指状突网状细胞和表皮棘细胞间LC和真皮浅层树突状网状细胞可表达HIT6-1抗原,并证实HIT6-1是CD1样McAb,并以此种McAb检测了12例SLE皮疹中LC,认为SLE皮疹中LC数目较正常者减少,而且形态也有异常.     

Prominent Langerhans' cell migration in the arthropod bite reactions simulating Langerhans' cell histiocytosis

BACKGROUND: Epidermal Langerhans' cells (LCs) play pivotal roles in cutaneous immune responses. An encounter with antigens or other stimuli causes the mobilization and migration of LCs. Therefore, some dermatoses, which originated from antigenic stimuli or trauma, can show LC migration. Recently, we experienced several cases of anthropod bites that showed marked inflammatory infiltrates with eosinophils and CD1a-positive LCs. It was difficult to differentiate these cases from Langerhans' cell histiocytosis (LCH). METHODS: The degree and pattern of LC infiltration in the skin of arthropod bite reaction was evaluated. The characteristics of CD1a immunohistochemical expression in the arthropod bite reactions were compared with those of LCH. RESULTS: A few arthropod bite cases (approximately 36%) showed extensive CD1a-positive LCs in the dermis, especially in the perivascular area. In addition, the CD1a expression patterns of LCs in the arthropod bite reactions were dendritic, whereas that of tumor cells in LCH were distinctly membranous and cytoplasmic. CONCLUSION: Some arthropod bite reactions can show marked CD1a-positive LCs in the dermis, especially in the perivascular area. The dendritic CD1a immunohistochemical staining pattern in arthropod bite reactions is useful in helping to differentiate from LCH.     

Ultraviolet B radiation suppresses Langerhans cell migration in the dermis by down-regulation of alpha4 integrin

Background/Purpose: Ultraviolet B (UVB) radiation affects the migration and function of epidermal Langerhans cells (LC) and causes immunosuppression of contact hypersensitivity. It is known that LC leaves the epidermis after exposure to UVB. To know the behavior of LC in the dermis after UVB radiation, we studied the effect of UVB radiation on the expression of integrin families on freshly isolated or cultured murine LC. We also examined whether UVB radiation affects the migration of LC to secondary lymphoid tissue chemokine (SLC/6Ckine).
Methods: Integrin expressions of murine LC cultured in epidermal cell suspension were analyzed using flowcytometry. We used murine LC sorted flowcytometrically for binding assay to extracellular matrix and for migration assay to chemokine. Skin explant assay and immnohistochemical staining for 'cords formation' were performed as previously described.
Results: Twenty and 40 mJ/cm² of UVB radiation down-regulated the expression of α4 integrin on 24 h-cultured LC, but not that of α6, β1, or β4 integrin. The number of cultured LC adhered to fibronectin, a ligand for α4 integrin, was decreased after UVB irradiation, while that to laminin, a ligand for α6 integrin, was not influenced. UVB radiation reduced the number of migrating LC to SLC. Furthermore, skin sheet explant experiments showed that UVB radiation inhibited the 'cords' formation in dermal vessels of the 48 h-cultured skin.
Conclusions: These data suggest that UVB radiation may suppress the migration of LC from the dermis to lymphatic vessels. UVB radiation may downregulate the adherence of LC to dermal fibronectin and migration to SLC, and consequently suppress the migration of LC from the UVB-irradiated dermis to lymphatics.     

Result of "as is patch test" using mite elements in atopic dermatitis (AD) patient. 2nd report, "Mite lipid"

The antigenicity of mite lipid was studied, taking atopic dermatitis as an allergic disease. Lipid was extracted from Dermatophagoides pteronyssinus (Dp) and D. farinae (Df). It was tentatively designated a mite lipid antigen (Dp-L, Df-L), and then a patch test was performed. An extract from animal food (LC) and acetone were used as the controls. With only Dp-L, a positive reaction of more than one plus (+) of the ICDRG standard was noted in 3 out of 21 cases of AD. Histology of the above-mentioned positive cases revealed spongiosis and infiltration of small round cells in the upper dermis along with scattered eosinophiles. Leu 6 positive cells were noted frequently in the epidermis and dermis. The lipid components of Dp-L were made up mostly of phospholipid and triglycerides+, and lipoprotein was not contained. Judging from the findings above it appears necessary to study not only protein but also lipid in connection with the mite antigenicity++ in AD in the future.     

A study of local immunity in psoriasis

We have studied biopsies of lesional skin with monoclonal and polyclonal antibodies to determine the nature of the infiltrate in different forms of psoriasis. In guttate psoriasis the number of Langerhans cells (LC) was not increased and CD8+ cells predominated, however, most CD4+ cells were activated. In erythrodermal psoriasis some CDI+ cells were found in the dermis although CD8+ cells predominated and were activated. In palmo-plantar psoriasis LC were found in the epidermis and superficial dermis and CD4+ cells were more numerous than CD8+ cells, some in turn expressing HLA-DR. In flexural psoriasis the LC formed clusters in the epidermis, and activated CD4+ cells predominated. In psoriasis vulgaris CD4+ cells predominated over CD8+ although the latter were activated. Our observations tend to support Valdimarsson's hypothesis on the immune basis of psoriasis, but we believe that two cycles coexist in psoriasis--one inflammatory and the other immunological--and that interaction between these leads to epidermal hyperproliferation.     

Langerhans cells in human warts

Seventy-six warts (15 plantar, 38 hand, 16 miscellaneous and seven anogenital lesions) taken from 55 patients, were studied by indirect immunofluorescence with monoclonal antibodies specific for T-cell subsets, Langerhans cells (LC) and HLA-DR antigen. The results were related to the presence of viral antigen. Approximately 80% of the lesions showed an infiltrate. Only 19 lesions contained helper/inducer or suppressor/cytotoxic T cells. The distribution of LC was abnormal in 65% of biopsies which contained LC in the dermis, and 29% were devoid of LC in the epidermis. Many lesions had reduced numbers of LC in the epidermis. The disappearance of LC from the epidermis was related to the presence of viral antigen, but not to the presence of particular T-cell subsets. Infiltrating cells were sometimes HLA-DR-positive, whereas basal cells did not express HLA-DR antigen, irrespective of the density of the infiltrate.     

Effect of granulocyte macrophage-colony stimulating factor on Langerhans cells in normal and healthy atopic subjects

Granulocyte macrophage-colony stimulating factor (GM-CSF) is a multipotent cytokine produced by many cutaneous cell types including keratinocytes. Langerhans cells (LC) represent the major antigen-presenting cells in skin, and in vitro studies demonstrate that GM-CSF is of pivotal importance in LC. Healthy volunteers ( n  = 3 non-atopic, n  = 3 with atopy) received recombinant human GM-CSF (0.05 μg/mL) by intradermal injection for 3 days to the same site. Diluent was injected in a similar manner as control. Biopsies were taken 24 h after the final injection and examined immunohistochemically for LC and inflammatory cell markers. Compared with control sites, intradermal GM-CSF resulted in shortening of dendritic cell processes and redistribution of LC in the epidermis; numbers of CD1a + cells in the epidermis were significantly decreased ( P  < 0.005), while those in the dermis were significantly increased ( P  < 0.05) following intradermal GM-CSF when compared with controls. Double labelling studies on epidermal CD1a + cells indicated de novo expression of intercellular adhesion molecule (ICAM)-1 and increased expression of HLA-DR following GM-CSF ( P  < 0.005, P  < 0.005, respectively). Additional findings included a marked mixed inflammatory cell infiltrate in the dermis and increased expression of the endothelial cell adhesion molecules E-selectin and ICAM-1. These data indicate that in normal human skin, GM-CSF induces changes in the phenotype and distribution of CD1a + cells consistent with LC functional maturation and exit from the epidermis to the dermis. As these events are central to the initiation of cutaneous inflammation, GM-CSF may potentially play a critical role in the pathogenesis of inflammatory dermatoses.     

Cutaneous dermal Ia+ cells are capable of initiating delayed type hypersensitivity responses

The presence of Langerhans cells (LC) within the epidermis has been shown to be critical for inducing T-cell-mediated immune responses in the skin. The purpose of this study was to assess whether cells in the dermis can initiate T-cell-mediated delayed-type hypersensitivity responses in vivo. Initially, back skins from C3H mice were trypsinized to remove the epidermis. The dermis was enzymatically dispersed and filtered to obtain a cell suspension. However, dermal cells exposed to trypsin were contaminated with numerous disaggregated hair follicles. These hair follicles contained Ia+ cells (presumably LC), and upon haptenation in vitro with trinitrophenyl, initiated contact hypersensitivity reactions in vivo. We therefore used dispase in place of trypsin to prevent follicular disaggregation and to allow preparation of dermal cell suspensions free of hair follicles. These hair follicle-free dermal cells were haptenated with trinitrophenyl and injected intradermally. Elicitation of contact hypersensitivity by epicutaneous painting 6 d later revealed the mean +/- SEM incremental ear-swelling response to be 53 +/- 8 mm X 10(-3). In contrast, mice sensitized by injection with dermal cells depleted of Ia+ cells demonstrated only 10 +/- 1 mm X 10(-3) of ear swelling. Thus, like dendritic LC of the epidermis, perivascular dendritic Ia+ cells of the dermis are capable of initiating T-cell-mediated contact hypersensitivity in vivo and may be highly relevant for presentation of antigen to T cells trafficking through the dermis.     

Fc gamma-receptor as a functional marker on epidermal Langerhans' cells in situ

Fc gamma-receptors (FcR) in cryostat sections of normal human skin were detected with soluble immune complexes of horseradish peroxidase (HRP) and rabbit IgG anti-HRP (HRP-anti-HRP). The binding of HRP-anti-HRP to Langerhans' cells (LC) was demonstrated using a double immunofluorescence staining in which LC were identified with a CD1a specific monoclonal antibody (Leu 6). The immune complexes gave granular staining of CD1a+ epidermal cells in sections of all specimens from normal skin. The mean percentage of CD1a+ cells that were FcR+ was 49 +/- 11 (n = 8). The FcR+/CD1a+ cells had a clearly defined dendritic pattern. The staining intensity of LC with HRP-anti-HRP was weaker than the intense staining of CD1a-macrophages in the dermis. Results of inhibition experiments indicate that human epidermal LC express low affinity FcR, but the presence of high affinity FcR as well cannot be excluded. The demonstration of FcR expression on normal LC clarifies previous uncertainty on LC membrane receptors, though the functional significance of these receptors is still not well understood.     

Migration of Langerhans cells into the epidermis of human skin grafted into nude mice.

In a previous study, it was demonstrated that human Langerhans cells (LC) are preserved in human skin grafted onto a nude mouse. Moreover, although it was observed that mouse LC of the host invade skin grafts from allogeneic mouse or rat, they do not penetrate in human skin grafts. In most of the human skin equivalent systems produced in vitro, LC appear to be lost. The present study was designed to investigate whether the mouse LC will repopulate a human skin equivalent. For this purpose, two different systems of skin equivalent have been grafted into the nude mouse. They were composed of human keratinocytes deposited on dead human dermis, or on lattice composed of human fibroblasts embedded in type I collagen. At different times after grafting, the presence of LC in the transplants was assayed either by indirect immunofluorescence or by electron microscopy. Indirect immunofluorescence was performed on frozen sections or on epidermal sheets with anti-Ia, anti-HLA-DR, or OKT6 antibodies. It was observed that, at 2 months after grafting, Ia(+) HLA-DR(-) OKT6(-) cells are present in grafted human epidermis. Moreover, LC with typical Birbeck granules are also detected by electron microscopy. It could be concluded, from this study, that mouse LC can repopulate human epidermis devoid of human LC.