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1.
为了探讨钙通道阻滞剂(CCBs)对迟发型超敏反应(DHR)的作用及其机制,我们观察了三类8种CCBs对小鼠变应性接触性皮炎(ACD)及表皮郎格罕细胞(LCs)影响。结果发现Ⅰ类CCBs异搏定、硫的氮酮,Ⅱ类CCBs尼莫地平、尼群地平及Ⅲ类CCBs佃嗪在抑制DHR的同时,亦减少表皮LCs数。提示上述药物可通过降低表皮LC数而抑制DHR。另外3种Ⅱ类CCBs心痛定、尼卡地平及络活喜亦显著抑制小鼠AC  相似文献   

2.
目的:为了探讨抗组胺药及抗5 羟色胺(5 HT)药对迟发型超敏反应(DHR)的作用及其机制。方法:我们观察了扑尔敏、特非那丁、多虑平、利血平、赛庚啶、苯噻啶对小鼠变应性接触性皮炎(ACD)及真皮肥大细胞(MC)、表皮郎格罕细胞(LCS)的影响。结果:发现这6种药物对小鼠ACD均有不同程度的抑制作用,提示这些药物的抗过敏作用不限于Ⅰ型变态反应疾病,对Ⅳ型变态反应疾病亦可有效。受试药物中扑尔敏、特非那丁、多虑平、利血平、赛庚啶等5种能减少真皮MC数,扑尔敏、多虑平、利血平等3种能减少表皮LCS数。结论:提示这些药物抑制DHR的机制至少部分地与减少真皮MC数及/或减少表皮LCS数有关。  相似文献   

3.
研究了不同浓度的1,25(OH)2维生素D(VD3)外涂对小鼠表皮郎格罕细胞(LC)的影响及对接触变态反应(CHS)的局部和系统抑制作用。结果表明随着1,25(OH))2VD3浓度的增加,LC树枝状减少,呈现卵圆或圆形细胞并且细胞数量下降。局部使用治疗剂量的1,25(OH)2VD3能直接抑制小鼠的CHS。并且,接受此种处理的小鼠脾细胞后,受体小鼠的CHS亦同样抑制。这提示与诱导体内抑制性淋巴细胞的  相似文献   

4.
对19例大疱性类天疱疮(BP)和5例获得性大疱性表皮松解症(EBA)病人进行了常规DIF、1mol/L NaCl分离表皮DIF和1mol/L NaCl分离正常人皮肤ⅡF的对比研究。结果显示1mol/L NaCl分离皮肤DIF染色法是诊断和鉴别诊断BP和EBA的一种简单、可靠、敏感的方法。  相似文献   

5.
为了揭示B细胞中CD23的表达与SLE发生发展的关系及在SLE发病机理中可能的作用,我们应用ABC免疫组化法和斑点核酸杂交技术对SLE患者外周血单一核细胞(PBMC)CD23蛋白和mRNA表达进行了检测。结果显示:30例SLE患者PBMCCD23蛋白表达显著增高(P<0.01),且与疾病活动呈正相关关系(rs=0.3814,P<0.05);具有不同ANA、抗dsDNA抗体水平,有无伴肾损、脑损的SLE患者,PBMCCD23表达均无显著性差异(P均>0.05);单纯使用皮质类固醇激素治疗或和其它免疫抑制剂联合治疗的SLE患者,PBMCCD23表达亦无显著性差异(P>0.05)。20例SLE患者PBMCCD23mRNA表达较正常人显著增高(P<0.01)。经治疗病情稳定后,CD23蛋白和mRNA表达均降至正常(P均>0.05)。提示在SLE活动期B细胞高度激活、增殖并大量表达CD23,且该种表达与ANA、抗dsDNA抗体产生水平无直接关系  相似文献   

6.
国产环孢素A对郎格罕细胞及接触过敏的影响   总被引:5,自引:1,他引:4  
环孢素A(CyA)作为非细胞毒免疫抑制剂,近年来广泛应用于某些皮肤病的治疗并取得较好的疗效。主要认为CyA能抑制CD+4T淋巴细胞及角朊细胞的增殖,但其全部作用机理尚未明了。最近研究发现CyA对银屑病患者郎格罕细胞、中性粒细胞、内皮细胞等亦产生影响[1]。郎格罕细胞作为皮肤抗原提呈细胞在接触过敏反应中起关键作用。有作者[2,3]分别报道CyA在体内、外均有减少和影响ATPase+LC数量及抗原提呈功能的作用。我们采用国产CyA对小鼠表皮LC及CHS两方面结合进行研究,观察其影响。一、资料和方法1…  相似文献   

7.
生殖器疣癌变过程中凝集素受体的分布   总被引:1,自引:0,他引:1  
应用生物素-抗生物素-酶标技术对BSL、DBA、LCA、PNA及UEA1在生殖器疣癌变过程中定位发现:PNA及UEA1受体在正常表皮阴性、PINⅢ/CINⅢ中等强度阳性及生殖器癌强阳性。另外,随着细胞异型性增加,BSL受体表达增强,DBA反而减少,LCA变化不显著。提示PNA及UEA1可制成探针用以区分生殖器疣与癌,其典型的染色特征可能提示重度非典型增生和恶性病变。  相似文献   

8.
紫外线辐射的尿刊酸对小鼠迟发型超敏反应抑制的研究   总被引:2,自引:1,他引:1  
建立了以小鼠耳厚的增加反映对DNP6-OVA抗原的迟发型超敏反应(DTH)的动物模型,以观察经紫外线辐射的顺式尿刊酸(cis-UCA)对小鼠DTH的抑制程度。结果注射cis-UCA的小鼠耳厚增加与对照组有显著性差异(尸<0.01),而注射反式尿刊酸(trans-UCA)的小鼠耳厚增加与对照无显著性差异(P>0.05)。表明在对DNP6-OVA的免疫应答中,cis-UCA能够抑制细胞免疫反应。  相似文献   

9.
对比观察60例SLE病人血浆脂质过氧化物(LPO)、红细胞超氧化物歧化酶(SOD)及过氧化氢酶(CAT)含量与ANA、ds-DNA、Sm和U1RNP自身抗体的变化。活动期病人活性氧基(OR)水平增高,以致SOD及CAT活性下降,LPO含量增高;非活动期SOD及CAT活性相对增高,LPO含量降低,提示体内OR水平下降。抗ds-DNA抗体滴度与红细胞SOD、CAT、血浆LPO含量及疾病的严重程度密切相关。内源性OR的增加可导致T抑制细胞功能下降,B淋巴细胞异常增殖,以致体内产生多种自身抗体,诱发免疫炎症反应  相似文献   

10.
牛脾转移因子及白三烯C4与异位性皮炎   总被引:1,自引:0,他引:1  
用牛脾转移因子口服液(OBS-TF)治疗异位性皮炎(AD)2 例,井采用3H放兔法测定了OBS-TF治疗前后AD患者及正常人血浆及外周血白细胞(PBL)中白三烯C4(LTC4)含量。AD血浆及PBL中LTC4含量治疗前均明显高于正常人,治疗后则无显著差异,AD的严重程度与LTC4水平相乎行,提示LTC4可能作为强效炎症介质之一介入了AD的发病过程, OBS-TF则可能作为LTC4的抑制剂对AD发挥了治疗作用。  相似文献   

11.
Abstract: In the guinea pig, experimental allergic contact dermatitis (ACD) And primary irritant contact dermatitis (PICD) were induced with different concentrations of dinitrochlorobenzene (DNCB). The epidermal Langerhans' cells (LCs) were observed sequentially by both adenosine triphosphatase (ATPase) and electron microscopy. Light microscopically, in ACD, the density and dendritic processes of LC decreased markedly within 12 h after antigen challenge. Almost no recognization LCs could be seen within 2 to 5 days. Later, LCs began to repopulale in the epidermis. Within 14 days, the density and shape of the LCs returned to normal. On the contrary, LCs changed more rapidly in PICD. The dendritic processes of LC decreased within 2 h and cell density decreased dramatically within 6 h after DNCB application. LCs also repopulated more rapidly in the epidermis. Electron microscopically, in ACD, we observed that lymphocyte-like cells apposed to LCs; LCs were activated and damaged; however, in PICD, we found neither the apposition of lymphocyte-like cells to LCs, nor the activation of LCs. LCs play an important role in the convalescence phase as well as in the early and later phases of contact allergic reaction.  相似文献   

12.
In the guinea pig, experimental allergic contact dermatitis (ACD) and primary irritant contact dermatitis (PICD) were induced with different concentrations of dinitrochlorobenzene (DNCB). The epidermal Langerhans' cells (LCs) were observed sequentially by both adenosine triphosphatase (ATPase) and electron microscopy. Light microscopically, in ACD, the density and dendritic processes of LC decreased markedly within 12 h after antigen challenge. Almost no recognization LCs could be seen within 2 to 5 days. Later, LCs began to repopulate in the epidermis. Within 14 days, the density and shape of the LCs returned to normal. On the contrary, LCs changed more rapidly in PICD. The dendritic processes of LC decreased within 2 h and cell density decreased dramatically within 6 h after DNCB application. LCs also repopulated more rapidly in the epidermis. Electron microscopically, in ACD, we observed that lymphocyte-like cells apposed to LCs; LCs were activated and damaged; however, in PICD, we found neither the apposition of lymphocyte-like cells to LCs, nor the activation of LCs. LCs play an important role in the convalescence phase as well as in the early and later phases of contact allergic reaction.  相似文献   

13.
Using OKT6 monoclonal antibody, we investigated the number of epidermal Langerhans' cells (LCs) in involved skin from patients with psoriasis, before and after mechlorethamine (HN2) or PUVA treatment. The number of LCs remained at about pretreatment number during three weeks of HN2 treatment alone, though they were reduced after 10 systemic PUVA treatments. Therefore, in contrast to PUVA which influences LCs, HN2 seems to have little effect on LCs. LCs in psoriatic plaques were, in number, 3-4 times less numerous than those in uninvolved, nontreated epidermis.  相似文献   

14.
An essential prerequisite for the in situ enumeration of epidermal Langerhans cells (LCs) is the unequivocal identification of the desired cell type. We have examined over 250 cryostat sections of normal human skin to analyze morphologic and methodologic problems underlying the quantification of epidermal LCs, defined by anti-T6 (OKT6) and anti-HLA-DR (OKIal) immunoperoxidase staining. Our findings show that OKT6 reactivity of dendritic processes in cross-sectioned epidermis yields microscopic images which are not easy to analyze objectively. The morphology that we find leads us to categorize dendritic cells into 3 arbitrary types of T6+ LC profiles. In addition we describe criteria for the assessment of OKT6 staining patterns relating to the dendritic state of epidermal LCs. Preliminary quantitative data on this issue are discussed in relation to: epidermal thickness; the thickness of skin tissue sections; and the discrepancy between the number of T6+ and HLA-DR+ LCs. We hope that the principles outlined in this report may serve to overcome potential methodologic problems with quantitation of T6+ epidermal LCs in skin sections.  相似文献   

15.
目的:观察几种抗组胺药对小鼠接触性皮炎的疗效及对表皮朗格汉斯细胞(LCS)数目的影响。方法:制作小鼠接触性皮炎模型,测量用药各组鼠左耳中部厚度变化及应用ABC免疫组化法测定LCS的数目。结果:对诱发皮炎前、后24h鼠耳厚度差的比较,咪唑斯汀组作用较强;各实验组与对照组比较,OX4 LCs、OX3*LCs均明显减少。结论:几种抗组胺药对小鼠迟发型超敏反应均有抑制作用,咪唑斯汀的作用较强;几种抗组胺药可使表皮LCs数目呈不同程度的减少;抗组胺药对迟发型超敏反应的抑制作用可能与LCs的数目减少有关,LCs数目的减少可能是其抑制迟发型超敏反应的机制之一。  相似文献   

16.
Trichloroacetic acid (TCA) peeling may be effective in solar lentigines, but with concerns regarding potential tumorigenesis. Cryopeeling would be better with improving the whole sun‐damaged skin. We aimed to compare the efficacy and safety of cryopeeling and TCA 35% peeling for treatment of solar lentigines and assess their influence on the number of epidermal Langerhans cells (LC). Twenty‐five patients were treated with TCA 35% and cryopeeling on the right and left hands, respectively. Two sessions were done 3 weeks apart. Evaluations were scheduled at weeks 0, 3, and 6. Skin biopsies, taken before and after treatment, were evaluated histologically and immunohistochemically for the number of CD1a + epidermal LCs. Lentigines decreased after cryopeeling from the first session (p < .001), but after the second session with TCA peeling (p = .004). Cryopeeling produced significant lightening, compared with TCA (p = .015). Blistering, hyper/hypopigmentation were reported with cryopeeling, whereas only hyperpigmentation was noted after TCA peeling. The LCs remained at about the pretreatment number after cryopeeling (p = .058), though they decreased after TCA (p = .002). Cryopeeling provided faster and superior improvement of lentigines compared with TCA peeling. Furthermore, TCA seems to suppress LCs raising the concern for carcinogenic potential.  相似文献   

17.
中药黄柏、茯苓及栀子抗迟发型超敏反应作用的实验研究   总被引:15,自引:0,他引:15  
本研究以小鼠 2、4 -二硝基氟苯 ( DNFB)变应性接触性皮炎 ( ACD)为迟发型超敏反应 ( DHR)的实验模型 ,分别以黄柏、茯苓及栀子的高、中、低剂量于致敏期及诱发期给药 ,观察鼠耳肿胀、耳部组织块重量。结果显示黄柏、茯苓及栀子均能明显抑制 ACD,且呈现一定量效关系 ,这对临床应用中药治疗以 DHR为主要发病机理的疾病具有指导作用  相似文献   

18.
To elucidate the etiological role of immunoglobulin molecules on Langerhans cells (LCs) in atopic dermatitis, we conducted immunohistochemical studies on the localization of immunoglobulin G1 (IgG1), IgG2, IgG3, IgG4, IgA and IgM on epidermal LCs from 30 patients with atopic dermatitis (AD) and five non-atopic healthy volunteers. We also investigated the types of receptors for the immunoglobulins (FcεRI, FcεRII, FcγRI, FcγRII, and FcγRIII) on epidermal LCs in the patients. IgE positive epidermal LCs were observed in 28 of 30 AD patients, and 46.7% of the epidermal LCs were positive for IgE. Both IgG1- and IgG2-positive epidermal LCs were obserbed in 70% of AD patients, and 21.8% and 28.7% of the total epidermal LCs were positive for IgG1 and IgG2, respectively. IgG3- or IgG4-positive LCs were present in only small proportions of AD patients. IgA-positive LCs were observed in 8 AD patients; our study suggested that the IgA bound on LCs was secretory IgA (S-IgA). These surface immunoglobulins were observed significantly more frequently on epidermal LCs in the involved skin of AD than in clinically uninvolved skin. No IgM-positive epidermal LCs were observed in the AD patients or healthy volunteers. In non-atopic healthy controls, no immunoglobulin-binding LCs were observed. In receptors for immunoglobulins, FcεRI and FcγRII were exclusively expressed on nearly all epidermal LCs from all AD patients and all non-atopic controls. These results suggested that not only IgE but also IgG and IgA may play some etiological role in the pathogenesis of AD.  相似文献   

19.
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