Plasma concentrations of sVCAM-1 and severity of dengue infections

Adhesion molecules are essential for the immune response. They are involved in the regulation of cell-to-cell contact, thereby enabling leukocytes to communicate. Circulating forms of adhesion molecules are found in the serum of healthy individuals. Raised levels have been associated with disease severity in HCV and other infections and thus appear to be good markers of endothelial damage. The levels of soluble Vascular Cell Adhesion Molecule-1 (sVCAM-1) and of sP and sL-selectin in the plasma of children hospitalised for dengue in French Polynesia were monitored. Studies from the 1996/1997 dengue-2 outbreak, showed that levels of sVCAM-1 increase steadily during the febrile period, peak on day 7, and then decline relatively rapidly. Disregarding the time frame within the febrile period, sVCAM-1 levels were always higher compared to controls. There was a significant association between sVCAM-1 levels and dengue haemorrhagic fever, a severe manifestation of dengue virus infection characterised by plasma leakage. No association was apparent between sVCAM-1 levels and primary vs. secondary dengue virus infections. Levels of sP-selectin and sL-selectin were significantly higher in primary compared with secondary infection but were not different in patients presenting with plasma leakage. Lastly, sVCAM-1 levels were significantly higher in an outbreak of severe disease in 1989/1990 (dengue-3) when compared to a non-severe outbreak in 1988/1989 (dengue-1) and a mild outbreak in 1996/1997 (dengue-2). The results suggested that levels of sVCAM-1 production might prove to be a useful marker in the management of severe dengue.     

Keratinocyte growth factor (KGF) decreases ICAM-1 and VCAM-1 cell expression on bronchial epithelial cells

Activation of leucocytes during airway inflammatory reaction involves adhesion to bronchial epithelial cells (BEC), a process implicating specific interactions between glycoproteins with epithelial cell surface proteins, mainly intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). In this study, the effect of keratinocyte growth factor (KGF), a growth factor involved in pulmonary epithelium repair, was evaluated on adhesion molecule expression with BEAS-2B cells and BEC and granulocyte adherence to BEAS-2B. The modulation by KGF of membrane and mRNA expression of ICAM-1 and VCAM-1 was studied on confluent cells stimulated or not with tumour necrosis factor-alpha (TNF) (200 UI/ml) or TNF and interleukin (IL)-4 (50 UI/ml and 10 ng/ml). Levels of soluble-(s)ICAM-1 and sVCAM-1 were measured by ELISA. Although moderately, KGF significantly decreased membrane ICAM-1 expression in unstimulated BEAS-2B cells (24% inhibition at 100 ng/ml) or in TNF- or TNF + IL-4-stimulated cells (22.5 and 18.7% inhibition, respectively). Treatment with KGF tended to decrease VCAM-1 expression in TNF- and TNF + IL-4-stimulated BEAS-2B (P = n.s. and P < 0.05, 14 and 15% inhibition, respectively). In primary culture of BEC, adhesion molecule expression was also reduced. ICAM-1 and VCAM-1 mRNA expression were also inhibited by KGF. Levels of sICAM-1 and sVCAM-1 were not significantly increased in supernatants from KGF-treated cells (30% and 24% increase at 100 ng/ml, respectively) compared to controls. Moreover, KGF decreased by 31% the adherence of neutrophils to TNF-activated BEAS-2B. In conclusion, KGF decreases ICAM-1 and VCAM-1 expression and neutrophil adherence in BEC. These suggest its involvement in the resolution of the inflammatory reaction.     

Inducible nitric oxide synthase (iNOS) and regulation of leucocyte/endothelial cell interactions: studies in iNOS‐deficient mice

It is well established that constitutive production of nitric oxide is central to numerous processes in the microvasculature, including controlling the trafficking of inflammatory leucocytes. However, during many inflammatory responses induction of inducible nitric oxide synthase (iNOS) increases nitric oxide production. The role of iNOS‐derived nitric oxide in modulating leucocyte recruitment is less well understood, although recent studies using iNOS‐deficient mice have begun to examine this issue. This article describes much of the work that implicates iNOS as having a role in controlling leucocyte recruitment, including the intravital microscopy studies which revealed that iNOS‐deficient mice have elevated leucocyte–endothelial cell interactions during endotoxaemia. Furthermore in additional studies, we compared expression of endothelial adhesion molecules in wild‐type and iNOS‐deficient mice, under conditions in which iNOS was expressed. Adhesion molecule expression was measured using an in vivo dual radiolabel immunoassay. To induce iNOS, mice were treated with either 1 or 50 μg of bacterial lipopolysaccharide (LPS), and 4 h later expression of P‐selectin, E‐selectin and vascular cell adhesion molecule‐1 was determined in eight different tissues. In nearly all cases, adhesion molecule expression did not differ between the two types of mice, either in the absence of an inflammatory stimulus, or following LPS treatment. These findings indicate that iNOS does not regulate expression of endothelial adhesion molecules either under basal conditions, or during the endotoxaemic response. This further suggests that alterations in leucocyte function may mediate the modulating effect of iNOS on leucocyte recruitment.     

Follicular dendritic cell (FDC)-FcgammaRIIB engagement via immune complexes induces the activated FDC phenotype associated with secondary follicle development

Follicular dendritic cell (FDC)-FcgammaRIIB levels are up-regulated 1-3 days after challenge of actively immunized mice with Ag. This kinetics suggested that memory cells are not driving this response, prompting the hypothesis that immune complex (IC)-FDC interactions lead to FDC activation. To test this, mice passively immunized with anti-OVA Ab were OVA challenged to produce IC. After 3 days, levels of IC, FcgammaRIIB, ICAM-1, and VCAM-1 on FDC were analyzed. FDC were also stimulated with IC in vitro, and mRNA for FcgammaRIIB, ICAM-1, and VCAM-1 was quantified by quantitative RT-PCR. IC labeling in passively immunized WT and FcgammaRIIB-/- mice revealed five to six FDC-reticula per LN midsagittal section. In WT mice, these IC-bearing FDC-reticula corresponded with FDC-reticula labeling for FcgammaRIIB, ICAM-1, and VCAM-1. Increases in these molecules on IC-stimulated FDC were confirmed by flow cytometry. In marked contrast, in FcgammaRIIB-/- mice, no increased VCAM-1 or ICAM-1 was seen on IC-bearing FDC-reticula or on purified FDC. Addition of IC in vitro resulted in dramatic increases in mRNA for FcgammaRIIB, ICAM-1 and VCAM-1 in WT FDC, but not in FDC from FcgammaRIIB-/- mice, 2.4G2-pretreated WT FDC, B cells, or macrophages. Thus, although FDC-FcgammaRIIB was not essential for IC trapping, engagement of FDC-FcgammaRIIB with IC initiated an FDC activation pathway.     

In vivo demonstration of T lymphocyte migration and amelioration of ileitis in intestinal mucosa of SAMP1/Yit mice by the inhibition of MAdCAM-1

The aetiology of Crohn's disease (CD) remains unknown. Since SAMP1/Yit mice have been reported to develop CD-like spontaneous enteric inflammation, such mice have been studied as an animal model of CD. In this study, using this model we examined T lymphocyte migration in microvessels of intestinal mucosa in vivo and the expression of adhesion molecules by immunohistochemistry. Fluorescence-labelled T lymphocytes isolated from AKR/J (control) mice were injected into the tail veins of recipient mice, and T lymphocyte migration in the postcapillary venules of Peyer's patches, submucosal microvessels, and villus capillaries of the terminal ileum was monitored using an intravital microscope. Adhesion of T lymphocytes was significantly increased in 35 week old SAMP1/Yit mice compared with that in AKR/J or 15 week old SAMP1/Yit mice. Immunohistochemical study showed increased infiltration of CD4, CD8 and beta7-integrin-positive cells and increased expression of MAdCAM-1 and VCAM-1 in the terminal ileum of SAMP1/Yit mice. Antibodies against MAdCAM-1 and VCAM-1 significantly inhibited adhesion of T lymphocytes to microvessels of the terminal ileum, and anti-MAdCAM-1 antibody showed stronger suppressive effect than the anti-VCAM-1 antibody. Periodical administration of anti-MAdCAM-1 antibody twice a week for 7 weeks significantly ameliorated ileitis of SAMP1/Yit mice, but submucosal hypertrophy was not significantly suppressed. Anti-VCAM-1 antibody treatment failed to show significant resolution of ileitis. In addition, anti-MAdCAM-1 antibody treatment also attenuated established ileitis. The results demonstrate that, although MAdCAM-1 and VCAM-1 play an important role in T lymphocyte-endothelial cell interactions in SAMP1/Yit mice, MAdCAM-1 may be a more appropriate target for therapeutic modulation of chronic ileitis.     

ICAM-1、P—selectin、D—dimer在子痫前期胎盘和血浆表达研究

目的探讨细胞间黏附分子（ICAM-1）、P-选择素（P—selectin）、D二聚体（D—dimer）在子痫前期发生发展中的作用。方法随机选取子痫前期患者39例为研究组,37例正常妊娠孕妇为对照组,采用免疫组织化学技术检测两组胎盘组织中ICAM-1、P—selectin的表达情况;采用酶联免疫吸附法（ELISA）检测两组血浆ICAM-1、P—selectin和D—dimer的表达水平。结果子痫前期组胎盘ICAM-1、P—selectin的表达明显高于对照组（P〈0．05）;两组血浆均有ICAM-1、P—selectin和D—dimer的表达,子痫前期组的血浆ICAM-1、P—selectin和D—dimer表达明显高于对照组（P〈0．05）。结论子痫前期患者ICAM-1、P—selectin和D～dimer表达升高可能与子痫前期的发生发展有关,监测这些指标对病情判断及指导治疗具有重要意义。     

Detection of mRNAs in Peyer's patches of the developing mouse embryo

We describe a method to identify cells expressing mRNA of interest in the developing digestive tract by whole mount in situ hybridization with digoxigenin-labeled RNA probes. In preparing samples, serosal tissue surrounding the intestine was removed. Enzymatic reactions and probe concentrations were optimized. Furthermore, polyvinyl alcohol was included in the reaction mixture for the color development of alkaline phosphatase conjugated to the antibody against digoxigenin. These modifications improved the sensitivity and enabled us to identity cells that express mRNA in embryonic intestine. Using the antisense probe for VCAM-1, the protein product of which is an immunohistochemical marker of the Peyer’s patch in the embryonic intestine, cells expressing mRNA were identified as spot-like clusters in Peyer’s patches, confirming the validity of the method. With this method, mRNAs of both lymphotoxins and β, key molecules for peripheral lymphoid organ development, were found to be confined to the Peyer’s patch in the developing intestine. Whole mount in situ hybridization analysis is a useful tool for exploring spatio-temporal expression profiles of mRNA in the developing immune organs.     

MCP—1对培养的人肾小球内皮细胞表达ICAM—1的影响

目的研究单核细胞趋化蛋白 - 1(MCP- 1)对培养的人肾小球内皮细胞 (HU GEC)表达细胞间粘附分子 - 1(ICAM- 1)的影响。方法采用细胞 EL ISA法。结果 1培养的 HU GEC表面有少量 ICAM- 1表达 ,在 10 ng/ m L MCP- 1刺激后 ICAM- 1表达量增多 (P<0 .0 5 ) ,6 h即有 ICAM- 1表达增强 ,12 h达高峰 ,不同浓度的 MCP- 1(10、2 0、40 ng/ m L)刺激HU GEC18h后 ,ICAM- 1表达与对照组比较差异显著 (P<0 .0 1) ;2加入抗 MCP- 1抗体后 ,ICAM- 1表达量下降 ,与对照组比较无差异 (P>0 .0 5 )。结论 MCP- 1可刺激 HU GEC表达 ICAM- 1增加。     

Human herpesvirus 6 infection of human epidermal cell line: pathogenesis of skin manifestations

In order to elucidate the pathogenesis of variant B human herpesvirus 6 (HHV-6) infection in skin tissues, an A431 cell line was inoculated with variant B HHV-6. HHV-6 causes abortive infection in the A431 cells, because neither late antigen (OHV-3 antigen) nor progeny virus is produced. Maximum levels of HHV-6 antigen (IEA/ex3 antigen)-positive cells (36.4%) were observed 48 hr after viral infection. Cocultivation of HHV-6-infected cord blood mononuclear cells with A431 cells was necessary for the establishment of a sufficient level of viral infection. Cell-to-cell contact between the infected cord blood mononuclear cells and A431 cells was crucial for increasing infection efficiency. To determine the biological effect of HHV-6 infection, flow cytometric analysis was carried out in HHV-6- and mock-infected A431 cells. Although no alteration was observed in VCAM-1 and ELAM-1 expression, that of HLA-ABC, HLA-DR, and ICAM-1 was upregulated after infection with HHV-6.     

PSGL‐1 and E/P‐selectins are essential for T‐cell rolling in inflamed CNS microvessels but dispensable for initiation of EAE

T‐cell migration across the blood‐brain barrier is a crucial step in the pathogenesis of EAE, an animal model for MS. Live cell imaging studies demonstrated that P‐selectin glycoprotein ligand‐1 (PSGL‐1) and its endothelial ligands E‐ and P‐selectin mediate the initial rolling of T cells in brain vessels during EAE. As functional absence of PSGL‐1 or E/P‐selectins does not result in ameliorated EAE, we speculated that T‐cell entry into the spinal cord is independent of PSGL‐1 and E/P‐selectin. Performing intravital microscopy, we observed the interaction of WT or PSGL‐1^?/? proteolipid protein‐specific T cells in inflamed spinal cord microvessels of WT or E/P‐selectin^?/? SJL/J mice during EAE. T‐cell rolling but not T‐cell capture was completely abrogated in the absence of either PSGL‐1 or E‐ and P‐selectin, resulting in a significantly reduced number of T cells able to firmly adhere in the inflamed spinal cord microvessels, but did not lead to reduced T‐cell invasion into the CNS parenchyma. Thus, PSGL‐1 interaction with E/P‐selectin is essential for T‐cell rolling in inflamed spinal cord microvessels during EAE. Taken together with previous observations, our findings show that T‐cell rolling is not required for successful T‐cell entry into the CNS and initiation of EAE.     

Abdominal peritoneum as a defense organ: Analysis of ICAM‐1 expression in the LPS‐stimulated rat

To investigate the immune environment of the peritoneal cavity, ICAM‐1 (intercellular adhesion molecule) expression on the apical surface of the hepatic peritoneum of LPS (lipopolysaccharide) stimulated rats was anlayzed ultrastructurally and chronologically with immnunoTEM&SEM. ICAM‐1 expression was restricted to the side of microvilli of the mesothelial cells. Microvilli demonstrated bulbous tips and included fuzzy coats and strands. Bulbous tips sometimes expressed the antigen, but fuzzy coats and strands did not. Intervillar cell surfaces lacked its expression. Although ICAM‐1 expression increased eightfold 24 hr after stimulation, the selective expression remained unchanged. These results suggest that microvilli are closely associated with cell migration in the peritoneal cavity through adhesion molecules that establish a road for migration. Clin. Anat. 12:20–26, 1999. © 1999 Wiley‐Liss, Inc.     

Adhesion molecules and atherogenesis

Atherosclerosis is an inflammatory disease of the vessel wall characterized by monocyte infiltration in response to pro‐atherogenic factors such as oxidized lipids. Recently, the role of specific adhesion molecules in this process has been explored. The endothelium overlying atherosclerotic lesions expresses P‐selectin and the shoulder regions express vascular cell adhesion molecule‐1 (VCAM‐1) and intercellular adhesion molecule‐1 (ICAM‐1), which is also expressed on endothelium in regions not prone to plaque development. Serum levels of soluble P‐selectin, ICAM‐1 and VCAM‐1 are elevated in patients with angina pectoris or peripheral atherosclerotic disease. Reconstituted in vitro systems using monocytes on cytokine‐activated endothelial cells under shear flow suggested the involvement of P‐selectin, L‐selectin, VCAM‐1, its ligand, VLA‐4 integrin and CD18 integrins. Studies of monocyte adhesion in isolated perfused carotid arteries harvested from atherosclerotic (apoE?/?) mice show a predominant involvement of P‐selectin and its ligand P‐selectin glycoprotein‐1 (PSGL‐1) in rolling and of VLA‐4 and VCAM‐1 in firm adhesion. Consistent with these findings, apoE?/? mice that are also deficient for P‐selectin show significantly reduced atherosclerotic lesion sizes and are almost completely protected from neointimal growth after vascular injury. Milder effects are also seen in the low‐density lipoprotein (LDL) receptor deficient (LDLR?/?) mouse. In a high cholesterol/cholate model, a role of ICAM‐1 and CD18 integrins was also shown, but this awaits confirmation in more physiologic models. Transient blockade of the VLA‐4/VCAM‐1 adhesion pathway by antibodies or peptides in apoE?/? or LDLR?/? mice reduced monocyte and lipid accumulation in lesions. These data suggest that P‐selectin, PSGL‐1, VLA‐4 and VCAM‐1 are the most important adhesion molecules involved in monocyte recruitment to atherosclerotic lesions.     

Phenotypic and functional characterization of CD11c+ dendritic cell population in mouse Peyer's patches

The antigen-presenting cell system in the gastrointestinal tract, one of three main sites (skin and lung being the others) of primary antigen contact, is poorly understood. Our study focused on dendritic cells (DC) as possible candidates for antigen uptake, processing and presentation in mucosal inductive sites, such as Peyer's patches (PP). To investigate the morphology, immunophenotype and stimulatory activity of intestinal DC, a procedure was developed to obtain a cell population by using collagenase digestion of PP, density centrifugation and cell sorting on the basis of CD11c expression. The resultant low-density cell fraction consisted of a nonadherent cell population expressing different intensities of CD11c that could at least be characterized by typical DC morphology (e.g. abundant cytoplasma with veil-like cytoplasmatic dendrites, irregularly shaped nuclei, multivesicular and multilamellar bodies), constitutive levels of surface MHC class II, the presence of macrophage-specific markers, such as F4/80, Mac-I and Fc receptors, respectively, on subpopulations of CD11c⁺ sorted cells and expression of adhesion and co-stimulatory receptors like ICAM-1 and CD44. The capability of this low-density CD11c⁺ fraction to stimulate T cell responses was demonstrated in primary allogeneic mixed-lymphocyte reactions (MLR). Herein, we show that the freshly isolated CD11c⁺ cells showed weak accessory function, but develop this capacity following short-term culture in vitro in the presence of granulocyte/macrophage colony-stimulating factor. Although the nature and functional capacity of the isolated CD11c⁺ needs further clarification, these preliminary results describing phenotype and accessory function provide some evidence that these cells isolated from the PP may be immature forms of DC and play a crucial role as antigen-presenting cells with important implications for understanding the complex network regulating intestinal antigen uptake, processing and presentation.     

Regulation of local and metastatic host-mediated anti-tumour mechanisms by L-selectin and intercellular adhesion molecule-1

Malignant melanoma is often accompanied by a host response of inflammatory cell infiltration that is highly regulated by multiple adhesion molecules. To assess the role of adhesion molecules, including L-selectin and intercellular adhesion molecule-1 (ICAM-1), in this process, subcutaneous primary growth and metastasis to the lung of B16 melanoma cells not expressing L-selectin, ICAM-1 or their ligands were examined in mice lacking L-selectin, ICAM-1 or both. Primary subcutaneous growth of B16 melanoma was augmented by loss of L-selectin, ICAM-1 or both, while pulmonary metastasis was enhanced by the loss of L-selectin or combined loss of L-selectin and ICAM-1. In both situations, the combined loss of L-selectin and ICAM-1 exhibited the greatest effect. This enhancement was associated generally with a reduced accumulation of natural killer (NK) cells, CD4+ T cells and CD8+ T cells and also with a diminished release of interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha but not interleukin (IL)-6. Cytotoxicity against melanoma was not defective by the absence of ICAM-1, L-selectin or both, suggesting that the enhancement of tumour growth and metastasis caused by the loss of adhesion molecules results from an impaired migration of effector cells into the tissue rather than from a suppression of the cytotoxic response. The results indicate that L-selectin and ICAM-1 contribute co-operatively to the anti-tumour reaction by regulating lymphocyte infiltration to the tumour.     

ICAM-1在着床期小鼠PBLC及EC/DC中表达的研究

目的：研究细胞间粘附因子－１（ＩＣＡＭ－１）在着床期外周血淋巴细胞（ＰＢＬＣ）、子宫内膜及蜕膜细胞（ＥＣ／ＤＣ）中的不同表达特点及动态变化规律。方法：以着床期小鼠为动物模型,细胞分析采用单抗免疫荧光标主多参数流式细胞术分析技术。结果：发现ＩＣＡＭ－１在ＰＢＬＣ、ＥＣ／ＤＣ中的均存在明显的动态变化;其中ＩＣＡＭ－１的表达在ＰＢＬＣ中于妊娠第２天（Ｄ２）达最低小平,而在ＥＣ／ＤＣ中于妊娠第４天（Ｄ４）     

Increased morbidity and mortality in murine cytomegalovirus-infected mice following allogeneic bone marrow transplant is associated with reduced surface decay accelerating factor expression

Infection with cytomegalovirus (CMV) remains a significant cause of morbidity and mortality following allogeneic bone marrow transplantation (allo‐BMT). The manifestations of CMV infection can range from neurological and haematological abnormalities to diminished graft survival and, in extreme cases, death. Many clinical studies have shown a direct correlation between cytomegalovirus infection and increased morbidity and mortality post allo‐BMT, yet the exact mechanism is not well understood. Although driven primarily by T cell responses, the role of complement activation in acute and chronic graft‐versus‐host disease (GVHD) has also become more evident in recent years. The present studies were performed to examine the effects of murine cytomegalovirus (MCMV) infection on decay accelerating factor (DAF) and MCMVs role in exacerbating morbidity and mortality post‐allo‐BMT. Mice infected previously with a sublethal dose of MCMV (1 × 10⁵ plaque‐forming units) have reduced expression of DAF on lung tissues and lymphocytes following allo‐BMT. More importantly, mortality rates post‐allo‐BMT in recipient DAF knock‐out mice receiving wild‐type bone marrow are increased, similar to wild‐type MCMV‐infected recipient mice. Similarly, DAF knock‐out mice showed greater intracellular interferon (IFN)‐γ production by lung CD8 T cells, and infection with MCMV further exacerbated both intracellular IFN‐γ production by CD8 T cells and mortality rates post‐allo‐BMT. Together, these data support the hypothesis that MCMV infection augments morbidity and mortality post‐allo‐BMT by reducing surface DAF expression.     

The angiogenic factor thymidine phosphorylase up-regulates the cell adhesion molecule P-selectin in human vascular endothelial cells and is associated with P-selectin expression in breast cancers

Thymidine phosphorylase (TP) is an angiogenic enzyme, catalysing the reversible phosphorylation of thymidine to thymine and 2-deoxyribose. TP is up-regulated in neoplasia, being associated with advanced tumour stage, microvessel density and prognosis in several tumour types. Although TP is a non-mitogenic migratory factor for endothelium, the mechanism by which TP mediates these effects is still unclear. We compared the gene expression profile of endothelial cells grown in vitro in the presence or absence of TP by cDNA microarray analysis. To determine the time-course of TP angiogenic induction, endothelial cells were stimulated with TP (10 ng/ml) for 5 and 18 h. Gene expression levels of Tie2, angiopoietin (Ang)1 and Ang2, measured by RNase protection assay (RPA), showed maximal alteration at 18 h. cDNA from human umbilical vein endothelial cells (HUVEC) grown for 18 h in the presence or absence of TP (10 ng/ml) was hybridized to a human cDNA cytokine array representing 375 angiogenic genes. Significantly altered expression occurred in 89 human angiogenic genes (72 genes were up-regulated and 17 down-regulated). Changes in five genes relevant to vascular remodelling biology (Tie2, nNos, P-selectin, ephrin-B1 and TP) were validated in triplicate experiments by real-time RT-PCR. But only P-selectin gene expression remained significant. Correlation between P-selectin and TP was assessed by immunohistochemistry on 161 human breast cancers, using human tissue microarray. Tumour cell TP correlated with tumour cell P-selectin but not with endothelial cell P-selectin. These data show that TP stimulates changes in mRNA expression maximally after 18 h culture in vitro. It confirms a role for TP in vascular remodelling involving several classes of genes, including the cell adhesion molecule, P-selectin. Although confirmation of the role of TP-mediated cell adhesion molecule (CAM) induction is required; however, this pathway may provide an attractive therapeutic target, since it is likely to affect several important tumour processes, including angiogenesis and metastasis.     

L-选择蛋白在小鼠肝癌细胞高低转移株HCa-F、HCa-P的表达及与肿瘤转移潜能的相关性

目的　探讨经淋巴道转移的小鼠肝癌细胞高低转移株HCa F、HCa P淋巴道转移能力及与淋巴细胞归巢受体L 选择蛋白的相关性。方法　应用免疫印迹分析、RT PCR及流式细胞术检测小鼠肝癌HCa F、HCa P细胞表面L 选择蛋白的表达情况 ,再通过E 、P 、L 选择蛋白的抗体对细胞粘附实验的影响检测HCa F、HCa P细胞淋巴道转移潜能与L 选择蛋白的相关性。结果　L 选择蛋白在HCa F、HCa P细胞表面均有表达 ,且HCa F细胞的表达量明显高于HCa P细胞 (P <0 .0 1) ,HCa F细胞与淋巴结之间的粘附可被抗L 选择蛋白的抗体所阻断。结论　小鼠肝癌细胞高低转移株HCa F、HCa P细胞均表达L 选择蛋白 ,其程度与该细胞的淋巴道转移潜能正相关     

Distribution of different cell types in the lymphoid organs of the mouse, as determined with sera against thymus and Peyer's patches

Anti-thymus serum (ATS) absorbed with Peyer's patch cells and anti-Peyer's patch serum (APS) absorbed with thymus cells were prepared. ATS treatment of mice resulted in a suppression of the immune response, measured with Vibrio cholerae as an antigen. APS did not have this effect. ATS and APS were used in the indirect fluorescence test to detect T and B_p cells. The cells staining with APS were called B_p cells to indicate that APS might only detect a special fraction of B cells (mature B cells). In Peyer's patches 66 per cent of the cells reacted with APS (B_p cells), whereas only 19 per cent cells reacted with ATS (T cells). The percentage of T cells in the lymph nodes was high (73 per cent), whereas only 14 per cent B_p cells were found in this organ. In the spleen almost equal numbers of B_p and T lymphocytes (32 per cent and 33 per cent) were detected. However, 35 per cent of the lymphocytes were non-reactive with either anti-serum. Bone marrow contained only small numbers of reactive cells (1 per cent T and 2 per cent B_p cells).

Treatment of mice with dimethylbenzanthracene (DMBA) caused an increase in the number of non-reactive cells in Peyer's patches and a dramatic decrease in the number of B_p cells. The relative increase of the number of T cells in spleen and lymph nodes was not found in Peyer's patches. Cortisone acetate seems also to act primarily on B cells, especially on those of Peyer's patches. In this case also an increase in the proportion of T cells in the spleen was detected.