Influence of Ethanol Consumption on Immune Competence of Adult Animals Exposed to Ethanol In Utero

Ethanol consumption results in significant changes in the immune system of experimental animals and humans. Previous work by ourselves and others has established that in utero exposure to ethanol results in alterations in the immune system of the offspring that persist into adult life. The present study was designed to determine if prenatal exposure to ethanol results in increased vulnerability to the immunosuppressive effects of ethanol consumption in adulthood. Male and female Sprague-Dawley offspring were selected in adulthood from prenatal ethanol (E), pair-fed (PF), and ad libitum-fed control (C) groups, and given either an ethanol-containing liquid diet or were pair-fed an isocaloric liquid diet without ethanol for 30 days. At the end of the 30-day feeding period, lymphocyte responses to the mitogens concanavalin A (Con A) and lipopolysaccharide, and to interleukin-2 (IL-2) were tested using in vitro assays. The results of this study support and extend previous data demonstrating long-term adverse effects of prenatal ethanol exposure on T-cell responses to mitogens, and provide further evidence that deficits seem to be more robust in male than in female offspring. Prenatal E males showed reduced T-lymphocyte proliferation to Con A and T-lymphoblast proliferation to IL-2, compared with their prenatal PF and C counterparts, regardless of whether they were exposed to the ethanol or the control diet in adulthood. In addition, T-lymphoblast proliferation to IL-2 was suppressed in prenatal E, compared with prenatal C, females exposed to control diet in adulthood. This is the first report of a deficit in T-cell aspects of immunity in E females, although it appears that this deficit may have been partially mediated by nutritional effects. A second major finding in this study is that consumption of ethanol diet in adulthood in itself had significant immunosuppressive effects on T-cell responses in both males and females. However, contrary to our expectation, previous exposure to ethanol in utero did not exacerbate the changes in immune responsiveness that were observed after adult ethanol consumption.     

中线外周T细胞淋巴瘤临床分析

目的分析中线外周Ｔ细胞淋巴瘤临床和病理情况。材料与方法本文回顾性分析自１９８６～１９９６年我院经病理证实的中线外周Ｔ细胞淋巴瘤３９例，原发部位鼻腔２７例、扁机体６例、鼻咽４例、软腭２例。其中放化综合治疗２５例，单纯放疗８例，化疗５例，未治１例。结果本组资料表明该病以男性为主，病变常累及多个部位，后期可广泛侵犯。Ｂ症状多，且易复发、进展，恶性度以中高度为主。单项治疗生存率为４０％，综合治疗６６．６７％，故应做放化综合治疗。如无颈部转移不须做颈部预防放射治疗。本病易短期复发、进展。结论本病恶性度高，作者认为要维持治疗以放化疗综合为主。     

T细胞亚群在再生障碍性贫血的变化

目的探讨再生障碍性贫血（ＡＡ）患者中Ｔ细胞亚群的变化。方法应用免疫酶标技术对１０例再障Ｔ细胞亚群测定与２０例健康人Ｔ细胞亚群含量进行比较分析。结果再障中ＣＤ３、ＣＤ４降低，ＣＤ８增多，ＣＤ４／ＣＤ８比值降低（Ｐ＜０．０５）。结论提示再障患者免疫平衡失调，免疫功能降低。     

特发性免疫球蛋白缺乏症继发外周T细胞淋巴瘤一例

目的 报道1例特发性免疫球蛋白缺乏症继发外周T细胞淋巴瘤。方法 通过病史、临床及实验室检查,病理及免疫组化以排除其他肿瘤性疾病,并观察临床用药治疗效果。结果 25岁男性患者的皮损呈丘疹、斑块及结节.发生于左臀部、上唇、鼻翼等部位。主要表现为反复发生的严重感染.IgG明显低于正常水平(<0.069 g/L)。皮损组织病理检查见真皮内大量大小不等的淋巴细胞。呈弥漫性分布.核异形,有丝分裂明显。皮损免疫组化检查.CD7、CD2、CD4、LAT均阳性,Ki-1、CD20、OCT2、CD56、CD68、CD79a均阴性。结论 本患者的诊断主要依据相关的实验室检查.临床表现是本病诊断的重要线索.有助于疾病的早期诊断。     

Reduced Alloreactive T-Cell Activation After Alcohol Intake is Due to Impaired Monocyte Accessory Cell Function and Correlates With Elevated IL-10, IL-13, and Decreased IFNγ Levels

BACKGROUND: Immunosuppression associated with chronic alcohol use is characterized by reduced antigen-specific T-cell response and impaired delayed type hypersensitivity. Increasing evidence suggests in chronic alcohol consumption models that reduced antigen-specific T-cell proliferation is due to insufficient accessory cell function. Accessory cell function, a critical step in recognition of viral antigens, is reduced in chronic hepatitis C. The severity of hepatitis C is increased by alcohol consumption. Thus, we investigated the effects of alcohol consumption on accessory cell activity of monocytes in supporting alloreactive T-cell proliferation. METHODS: Alloreactive T-cell proliferation was evaluated in a one-way mixed lymphocyte reaction (MLR). Mononuclear cells were isolated by Ficoll density gradient and monocytes by adherence. Alcohol (0.8 g/kg body weight, an equivalent of approximately three drinks) was given to nonalcohol-consuming individuals and blood samples were collected before, 4 hr, or 18 hr after alcohol consumption. Alcohol in vitro was administered at concentrations of 25-100 mM. RESULTS: T-cell proliferation in MLR was significantly reduced in the presence of physiologically relevant concentrations of alcohol in vitro (25-100 mM ethanol) (p < 0.05). In vivo alcohol consumption also depressed proliferation in the MLR when stimulator cells were obtained 4 hr after alcohol consumption. MLR was not decreased, however, in the presence of alcohol-exposed responder cells and normal stimulator cells, suggesting that the accessory cell population and not T cells are affected by alcohol. Decreased accessory cell function was further evidenced by reduced superantigen-induced (SEB) but not mitogen-induced (PHA) T-cell proliferation in samples obtained 18 hr after alcohol intake (35% reduction). Reduced accessory cell function was not due to changes in surface expression of monocyte costimulatory molecules (HLA class I, HLA-DR, CD80, CD86, CD40). We found reduced IFNgamma, elevated IL-10, and unchanged IL-4 levels during T-cell proliferation in samples obtained 18 hr after alcohol consumption. Acute alcohol treatment resulted in increased IL-13 in the MLR. CONCLUSION: These data suggest that even on one occasion moderate alcohol intake can reduce allostimulatory T-cell activation via decreasing accessory cell function. Increased IL-10 and IL-13 plus the reduced IFNgamma production after acute alcohol use are likely to contribute to both the reduced T-cell proliferation and monocyte accessory cell function. These accessory cell mediated defects in T-cell activation may result in impaired antiviral and antitumor immunity after moderate acute alcohol use.     

Distribution of T-cell subpopulations in the peripheral blood of patients with erythrodermic psoriasis

Summary In the present study the percentages of T cells and T-cell subsets, as defined by Fc receptors and monoclonal antibodies (OKT3, OKT4, OKT8, HLA-DR were determined in the peripheral blood of 12 patients with psoriasis, including six patients with erythroderma and 6 with active, but limited disease. The patients with erythroderma were studied before treatment and 4–8 weeks following.The mean percentages of E-rosette-forming cells and T-cell subsets reactive with the monoclonal antibodies OKT3, OKT4 and OKT8 were within normal limits, as were the percentages of T-cells, irrespective of the extent or activity of the disease. The mean percentage of T-cells was reduced in the patients with untreated erythrodermic psoriasis but not in the patients with limited disease. Comparison of the T values in the erythroderma group before and after therapy showed a slight, but statistically significant increase (P<0.03). These results indicate a direct relationship between the T deficit and the extent of skin involvement, and argue against a primary suppressor T-cell defect in psoriasis vulgaris.     

NK/T细胞淋巴瘤误诊1例分析并文献复习

目的：提高对NK/T细胞淋巴瘤临床病理特征的认识。方法：对1例NK/T细胞淋巴瘤进行分析,并结合文献其临床病理特点。结果：NK/T细胞淋巴瘤是一种少见的恶性淋巴瘤。结论：NK/T细胞淋巴瘤的诊断主要依据临床表现、组织学特点、免疫组化表达。     

Frequent Development of Murine T-Cell Lymphomas with TcRα/β+, CD4-/8 Phenotype after Implantation of Human Inflammatory Breast Cancer Cells in BALB/c Nude Mice

Tumors developed quite frequently in some of the visceral organs, including spleen and liver, in BALB/c nude mice upon subcutaneously xenografting surgical specimens from five different inflammatory breast cancer patients. All of these tumors developed within two and a half months to one year after the subcutaneous inoculation of surgical specimens. From these tumors, five independent transplantable tumors, including tMK-2, tHK-1, tYK-1, tYK-2 and tTY-1 have been established. Chromosome analysis, morphologic studies by light and electron microscopy and phenotype analysis indicated that these tumors are of mouse origin. The tMK-2 tumor was highly metastatic to the spleen and liver when it was subcutaneously transplanted into the right scapular region. In addition, the region where the tMK-2 tumor cells were subcutaneously inoculated showed an apparently inflammatory process represented by erythema. After subcutaneous inoculation into the right scapular region, tHK-1, tYK-1,2, and tTY-1 tumors also metastasized to some of the visceral organs, including spleen and liver. From these tumors, in vitro cell lines were established. The cells grew in a stromal-cell dependent manner under in vitro culture conditions. The cells were again tumorigenic at the inoculated region and metastasized to various organs, including liver and spleen, of BALB/c nude mice. Histological examination revealed that the tumors showed features of malignant lymphoma. Phenotypically, these five tumors expressed early T lymphocyte markers as revealed by anti-mouse anti-TcR4aL/β, anti-CD3, CD4 and CDS monoclonal antibodies. To our knowledge, these cell lines are the first T-cell lines showing the phenotype of extrathymically differentiated T-cells in the liver.