IFN-α Acts on T-Cell Receptor-Triggered Human Peripheral Leukocytes to Up-Regulate CCR5 Expression on CD4+ and CD8+ T Cells

Interleukin-12 (IL-12) as well as IL-2 was recently shown to up-regulate CCR5 expression on T-cell receptor (TCR)-triggered human T cells. Because of the functional similarity between interferon-alpha (IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">) and IL-12, the present study investigated whether IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> also up-regulates T cell CCR5 expression. CCR5 was marginally detected on T cells from unstimulated human peripheral blood leukocytes (PBLs) and only slightly induced on PBL T cells following stimulation with anti-CD3 plus anti-CD28 monoclonal antibodies (mAbs). When anti-CD3/anti-CD28-triggered PBLs were exposed to IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">, T cells expressed high levels of CCR5. The levels of CCR5 expression were comparable to those induced by IL-12. However, when purified T cells instead of unfractionated PBL were stimulated with anti-CD3/CD28 and then exposed to IL-12 or IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">, CCR5 expression was induced by IL-12 but not by IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">. IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> was found to act on anti-CD3/anti-CD28-stimulated PBL to promote their IL-12 production. Moreover, addition of anti-IL-12 mAb to IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">-stimulated cultures of anti-CD3/CD28-pretreated PBL resulted in considerable inhibition of CCR5 expression. Together, these results indicate that IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> as well as IL-12 up-regulates CCR5 expression on TCR-triggered T cells and that IFN-rh328n6587l79714/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> functions not by acting directly on T cells but via enhancing IL-12 production by PBL.     

重组红细胞生成素对血透患者免疫功能的影响

目的：评价重组红细胞生成素（ｒＨ－ＥＰＯ）对透析患者免疫功能的影响。方法：用流式细胞仪、双抗体夹心酶标法、ＥＬＩＳＡ法、ＭＴＴ比色法以及淋巴细胞毒试验检测接受ｒＨ－ＥＰＯ治疗的慢性血透患者以及透析治疗不伴贫血患者的淋巴细胞亚群、细胞因子等免疫指标。结果：治疗组ｒＨ－ＥＰＯ治疗前淋巴细胞亚群、细胞因子与正常人、患者对照组比较有显著性差异（Ｐ〈０．０５）。治疗组ｒＨ－ＥＰＯ治疗前后ＣＤ３、细胞因子、淋     

rhIL-12 as adjuvant augments lung cell cytokine responses to pneumococcal whole cell antigen

Conjugate pneumococcal vaccines offer suboptimal protection against mucosal infections and are restricted in serotype and geographical coverage. New protein-based vaccines using conserved pneumococcal antigens and better mucosal adjuvant technology are urgently needed. Interleukin-12 (IL-12) has shown efficacy as a pneumococcal protein vaccine adjuvant in murine models of pneumococcal infection. Systemic administration of recombinant human (rh) IL-12 to humans, however, has been associated with adverse clinical and laboratory side effects. Inhaled forms of IL-12 have improved the safety profiles in humans, as suggested by animal models. Here we evaluated rhIL-12 as an adjuvant on ex vivo human BAL cells when stimulated with pneumococcal whole cells. We show that co-incubation of ex vivo human BAL cells with pneumococcal whole cell antigen (WCA) and a low dose of rhIL-12 (2 ng) can elevate TNF production compared to treatment with WCA (p = 0.06) or rhIL-12 (p = 0.03) alone. The production of IFNγ was also increased but not in an antigen specific manner, suggesting perhaps a predominant Th₁ response. Our data suggest that 100-200-fold lower doses of inhaled rhIL-12 than those previously tested for systemic use may be adequate in a phase 1 study and commend further evaluation of rhIL-12 as a potential mucosal adjuvant in human vaccine studies.     

Atypical antipsychotics suppress production of proinflammatory cytokines and up-regulate interleukin-10 in lipopolysaccharide-treated mice

There is considerable evidence that schizophrenia is associated with immune system dysregulation. For example, blood and cerebrospinal fluid (CSF) levels of proinflammatory cytokines are significantly increased in schizophrenic patients, and their normalization correlates with improvement in psychotic symptoms. In fact, typical and atypical antipsychotics are reported to modulate immune function in in vitro and in vivo studies. In the present study, we examined the anti-inflammatory effect of antipsychotics, clozapine, olanzapine, risperidone and haloperidol, on serum cytokine levels in lipopolysaccharide (LPS)-treated mice. Atypical antipsychotics, such as clozapine, olanzapine and risperidone, but not haloperidol, suppressed tumor necrosis factor (TNF)-α and interleukin (IL)-6, and up-regulated IL-10. Moreover, only clozapine, robustly increased the serum levels of IL-10. Clozapine reproduced its anti-inflammatory feature in polyinsinic–polycytidylic acid sodium salt (Poly[I:C])-induced inflammation. Thus, the anti-inflammatory effect of clozapine would adapt to inflammation induced by some varieties of antigens. Several receptor ligands, such as 8-OH-DPAT, ketanserin, prazosin and scopolamine, were also examined as to their anti-inflammatory effects on serum cytokine levels in LPS-treated mice. Ketanserin and prazosin, but not 8-OH-DPAT nor scopolamine, behaved similarly to atypical antipsychotics. However, the remarkable increase of serum IL-10 level observed in clozapine was not detected in ketanserin and prazosin. These results suggest the unique efficacy of atypical antipsychotics in the suppression of proinflammatory cytokines, and the increase of anti-inflammatory cytokine, IL-10.     

2009年～2011年陕西省临床血型鉴定室间质量评价分析

目的:探讨临床血型鉴定室间质量评价错误的原因。方法:分别统计2009年、2010年和2011年陕西省临床检验中心临床血型室间质量评价活动结果。结果:2009年全省正鉴定参评单位133家,ABO正鉴定错误单位为1家,占参评单位的0.75%,Rh血型鉴定错误单位为1家,占参评单位的0.75%,血型反鉴定参评单位126家,反鉴定错误单位为8家,占参评单位的6.35%;2010年全省正鉴定参评单位192家,ABO正鉴定错误单位为1家,占参评单位的0.52%,Rh血型鉴定错误单位为1家,占参评单位的0.52%,血型反鉴定参评单位190家,反鉴定错误单位为7家,占参评单位的3.68%;2011年全省正鉴定参评单位200家,ABO正鉴定错误单位为1家,占参评单位的0.5%;Rh血型鉴定错误单位为1家,占参评单位的0.5%,反鉴定参评单位195家,反鉴定错误单位为14家,占参评单位的7.18%。ABO血型鉴定错误主要表现在反向反应。结论:ABO试剂红细胞质量是引起血型错误主要原因。     

重组人睫状神经营养因子干预家兔视神经损伤动物模型视神经蠕变特性的分析

以蠕变特性指标研判重组人睫状神经营养因子干预动物视神经损伤的效果。以钳夹法复制动物视神经损伤模型,以重组人睫状神经营养因子连续干预30 d后,对各组动物进行视觉电生理检测,之后取各组动物视神经进行组织形态观察和蠕变实验。视神经损伤模型以重组人睫状神经营养因子干预治疗组Pl峰值大于视神经损伤模型组,差异显著(P0.05)。以重组人睫状神经营养因子干预治疗组视神经纤维结构尚存,较少部分视神经纤维排列不规则,视神经无明显变细,视神经损伤模型组兔视神经纤维束结构消失,神经纤维和胶质细胞变性、坏死。视神经损伤以重组人睫状神经营养因子干预治疗组7 200 s应变上升量大于视神经损伤模型组组、差异显著(P0.05)。以重组人睫状神经营养因子干预治疗动物视神经损伤模型后视神经的织形态、蠕变特性等得到较大的恢复。     

重组人红细胞生成素治疗肾性贫血的疗效分析

目的:探讨不同透析方式影响重组人红细胞生成素的疗效。方法:75例病人分为血液透析、腹膜透析、无透析三组。分别在用药前后测定三组病人的贫血程度(血红蛋白、红细胞、红细胞压积)。结果:同组病人用药前与用药8周后的贫血程度有显著差异性(P<0.01),但三组之间对比无差异性(P>0.05)。结论:提示重组人红细胞生成素治疗肾性贫血有明显效果,但不同透析方式不影响其疗效。