针刺对豚鼠血淋巴细胞阿片样肽免疫组织化学反应影响的研究

本文报道对64只豚鼠的血淋巴细胞,分别在电针、给予纳洛酮或外源性阿片样肽(OLP)等不同条件下,以PAP免疫组织化学法显示甲脑啡肽(MEK)、亮脑啡肽(LEK)及β-内啡肽(β-EP)的免疫反应(IR)。另对部分免疫组织化学标本,随后显示酸性非特异性酯酶(ANAE)。约96％的血淋巴细胞呈强弱不等的OLP阳性反应。甲脑啡肽强阳性反应淋巴细胞(MEK-IIRL)和β-EP强阳性反应淋巴细胞,与ANAE的点型淋巴细胞,均呈显著正相关;但LEK强阳性反应淋巴细胞与ANAE的点型淋巴细胞的相关不显著。电针豚鼠“足三里”穴后,MEK、LEK及β-EP的强阳性反应淋巴细胞计数均显著提高。将电针组、纳洛酮组和对照组的结果做比较,见3组间的OLP(包括脑啡肽和内啡肽)的强阳性反应淋巴细胞计数差别皆不显著。但当分别加10~(-7)mol/L MEK、LEK和β-EP体外孵育淋巴细胞后,纳洛酮对OLP强阳性反应淋巴细胞有抑制效应,纳洛酮组和电针组的OLP强阳性反应淋巴细胞计数均呈显著差异。在外加10~(-12)～10~(-3)mol/L MEK体外孵育淋巴细胞后,可见电针组比对照组在10~(-10)～10~(-3)mol/L浓度间MEK免疫反应呈现一个明显高峰,提示电针可能提高潜在未结合的MEK受体的活性。     

登革Ⅱ型病毒对淋巴细胞和骨髓细胞SCE率影响的实验研究

报道３０例离体培养的人体外周血淋巴细胞及２０例离体培养的正常人骨髓细胞加入登革Ⅱ型病毒前后的ＳＣＥ率改变，结果表明：登革Ⅱ型病毒可以提高外周血淋巴细胞及骨髓细胞的ＳＣＥ率，说明该病毒对人体这两类细胞的染色体均具有损伤作用。实验还观察到不同个体的淋巴细胞及骨髓细胞在加入登革Ⅱ型病毒后，其ＳＣＥ率的升高有个体差异，说明了染色体或ＤＮＡ损伤程度不等。     

Double fluorescence technique for measurement of complement-fixing antibody to lymphocyte subsets

A double fluorescent antibody method for quantitating human complement-fixing antibody to lymphocyte subclasses has been developed. The indicators in this system are a C6-deficient serum as a non-lytic source of complement, rhodamine-labeled anti-C3 and fluorescein-labeled murine monoclonal antibodies to human lymphocyte subsets. The basic procedure is to incubate lymphocytes with the unknown serum and then to add C6-deficient serum. The binding of C3 is indicated by staining with rhodamine-labeled anti-C3 and the subset class of the lymphocyte so stained is determined by binding of fluorescein-tagged anti-OKT4 or -OKT8 antibodies. The occurrence of both red and green cell surface fluorescence denotes the presence of a complement-binding antibody to the lymphocyte subset defined by the monoclonal antibody. In addition to defining the specificity of complement-fixing anti-lymphocyte antibodies, this technique is more sensitive than the microcytotoxicity assay.     

A comparison of methods for enumerating lymphocyte classes

We have evaluated a novel kit method for enumerating B and T lymphocytes using antibody-coupled beads. The technique proved to be an unsuitable alternative to sheep red blood cell rosettes and immunofluorescence. However, the principle is potentially valuable and we suggest certain modifications which would make the method more suitable for routine use.     

匹多莫德预防过敏性紫癜复发的42例临床观察

目的观察匹多莫德预防过敏性紫癜（HSP）复发的临床效果及相关因素分析。方法78例HSP患儿随机分为治疗组42例和对照组36例,30例健康儿童作为正常对照组。对照组常规治疗,治疗组加匹多莫德颗粒剂口服。观察住院期间、2个月内、6个月内的反复、复发率及测定治疗前、治疗2个月时血CD3＋、CD4＋、CD8＋、白介素-2（IL-2）、γ-干扰素（IFN-γ）水平。结果HSP患儿治疗前血CD3＋、CD4＋、IL-2、IFN-γ水平均低于正常对照组（P均〈0.01）,CD8＋细胞水平各组间无差异（P〉0.05）;治疗2个月后治疗组血CD3＋、CD4＋、IL-2、IFN-γ水平较对照组明显上升（P〈0.01或P〈0.05）,与正常对照组无显著差异（P〉0.05）;住院期间治疗组的反复率与对照组比较无显著性差异（P〉0.05）;2个月及6个月内治疗组的复发率明显低于对照组（P〈0.05）。结论匹多莫德能降低HSP患儿的复发率,可能与其对HSP患儿T细胞功能的调整密切相关。     

Cell cooperation in development of eosinophil-predominant inflammation in airways

A large body of research supports a pathogenic role of Th2 cells in allergic diseases such as asthma. These disorders are characterized by recruitment to selected peripheral tissues of a mixed leukocyte inflammatory infiltrate including a predominant e osinophil component. The development of this inflammatory response is dependent on accumulation of Th2 cellsin the affected tissues. Our studies aim to define the mechanisms that control the development of this tissue inflammatory response, focusing particularly on the mechanisms that recruit Th2 cells to the lung and airway. We have found that Th2 cells are their own poorly competent for antigen-induced recruitment to the lung. By contrast, Th1 cells are avidly recruited to the lungs in response to airway antigen challenge. More important, recruitment of Th1 cells to the lung resulted in enhanced recruitment of Th2 cells to this tissue. The increased. Th1 cell-induced recruitment of Th2 cells was associated with upregulation of endothelial vascular cell adhesion molecule-1 (VCAM-1) expression in airway-associated endothelial cells and could be largely blocked by systemic treatment with a monoclonal anti-VCAM-1 antibody. Systemic blocking of tumor necrosis factor (TNF) also blunted the airway inflammatory response. The prominent roles of TNF and VCAM-1 in recruitment of Th2 cells suggested that an inflammatory microenvironment was essential for the recruitment of Th2 cells. Infact, recruitment of Th2 cells to the airway could be induced in an antigen-independent fashion by proinflammatory stimuli such as intranasal in stillation of endotoxin. This antigen nonspecificity of the Th2 cell recruitment suggested a model in which Th2 cell recruitment is in response to general inflammatory signals rather than to antigen itself. This model provides an explanation for the clinical observation that bacterial or viral respiratory tract infections are associated with disease exacerbations in allergic asthmatics. More generally, these data imply that Th2 cells, like other leukocytes, are recruited efficiently to site of tissue inflammation, and that these nonspecifically recruited Th2 cells have substantial potential to modulate local inflammatory processes.     

Heterogeneity in P-glycoprotein (multidrug resistance) activity among murine peripheral T cells: Correlation with surface phenotype and effector function

P-glycoprotein (P-gly) is the transmembrane efflux pump responsible for multidrug resistance in tumor cells. Functional P-gly activity can be conveniently assessed microfluorometrically using the fluorescent dye rhodamine 123 (Rh123), which is an artificial substrate for the P-gly transporter. Here we assess P-gly activity in subsets of mouse peripheral T lymphocytes using the Rh123 efflux assay. Our data indicate that virtually all CD8⁺ cells extrude Rh123 efficiently, whereas only a subset of CD4⁺ cells exhibit P-gly activity. Correlation of P-gly activity in CD4⁺ cells with the expression of a panel of surface markers revealed that cells bearing an “activated/memory” phenotype (CD45RB^?, CD44^hi, CD62L^?, CD25⁺, CD69⁺) were exclusively found in the fraction that can extrude Rh123. In contrast “naive” phenotype CD4⁺ cells (CD45RB⁺, CD44^lo, CD62L⁺, CD25^?, CD69^?) could be further subdivided into two major subsets based on P-gly activity. In functional studies of sorted cell populations the Rh123-extruding subset of “naive” CD4⁺ cells proliferated more strongly and secreted higher levels of interleukin (IL)-2 than its Rh123-retaining counterpart when activated by a variety of polyclonal stimuli. Furthermore, this subset produced detectable levels of interferon (IFN)-γ upon stimulation but no IL-4 or IL-10. As expected, the Rh123-retaining “naive” subset produced only IL-2 after stimulation, whereas the “memory” subset produced IFN-γ, IL-4 and IL-10 in addition to low levels of IL-2. Collectively, our data indicate that P-gly activity is a novel parameter that can be used to distinguish a subset of “preactivated” CD4⁺ cells that would be considered as naive on the basis of their surface phenotype.     

CD23 defines two distinct subsets of immature B cells which differ in their responses to T cell help signals.

Transitional immature B cells undergo apoptosis and fail to proliferate in response to BCR cross-linking, thus representing a target for negative selection of potentially autoreactive B cells in vivo. In agreement with recent reports, transitional B cells were divided into developmentally contiguous subsets based on their surface expression of CD23. When transferred, CD23(+) transitional B cells readily localized to the splenic follicles and the outer PALS. Compared with CD23(-) transitional B cells, CD23(+) transitional B cells proliferated more vigorously and were rescued from BCR-induced apoptosis to a greater degree, by T cell help signals. However, both CD23(-) and CD23(+) transitional B cells failed to up-regulate CD86 (B7-2) in response to BCR ligation. These findings demonstrate that phenotypically defined subsets within the transitional B cell population are functionally distinct. Specifically, responsiveness to T cell help is a late acquisition corresponding to the stage when the B cells gain access to peripheral compartments enriched in antigen and activated T cells. The failure of transitional B cells to up-regulate CD86 to BCR-mediated stimulation suggests a unique interaction between transitional B cells and T cells with implications for tolerance in the T cell compartment.     

Unraveling the origin of lymphocyte progenitors

Lymphocytes are ultimately derived from hematopoietic stem cells, however the intervening steps that give rise to lymphocyte progenitors are still under intense investigation. In particular, whether a common lymphocyte progenitor serves exclusively as a lymphoid precursor, or whether this cell retains limited myeloid progenitor potential are addressed by Rolink and colleagues. This issue is highlighted by their identification within the bone marrow of early progenitors with lymphoid and myeloid developmental potential or EPLMs. How these cells fit into our current understanding of lymphocyte development, and how this new subset helps to further refine our view of the common lymphocyte progenitor are discussed.     

Self-Reactivity and the Expression of Memory Markers Vary Independently in MRL-Mp+/+ and MRL-Mp-lpr/lpr Mice

MRL-Mp-lpr/lpr mice contain phenotypically abnormal populations of T cells, and exhibit an SLE-like autoimmune disease in which autoantibodies are a prominent feature. We analyzed the phenotype and T-cell receptor Vß expression pattern in CD4⁺ T cells of this mutant mouse strain to detect abnormalities that could explain the autoimmunity. The CD4⁺ T cells contain two distinct abnormal populations. One of these expresses B220 and HSA, and in these and other respects closely resembles the accumulating CD4^–CD8^– population. The other expresses a high level of CD44 (Pgp-1), and a high level of the 16A epitope of CD45, and so resembles post-activation T cells. Both of these cell types are exclusive to MRL-Mp-lpr/lpr. We also identified V ß5- and V ß11-positive CD4+ T cells, in both MRL-Mp-lpr/lpr and MRL-Mp-+/+ mice. We conclude that autoimmune T cells can be detected in these mice, but that they are not the cause of the accumulation of abnormal CD4⁺ and CD4^–CD8^–cells.