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1.
目的:探讨模拟固壳未破损失事潜艇环境条件暴露对人体血液免疫功能的影响及其变化的规律。方法:使用500m饱和潜水居住舱系统模拟失事潜艇固壳未破损舱室环境条件,控制舱内温度、PCO2、PO2,于进舱前、暴露第2、4、8d采晨空腹血,用流式细胞分析术测定红细胞、淋巴细胞、中性粒细胞表面CD55和CD59的分布变化。结果:红细胞膜表面CD55的分布在8d有显著升高(P〈0.01);淋巴细胞膜表面CD55的分布在暴露的初、中期显著下降(P〈O.01),后期明显恢复,与温度、PO2呈正相关(P〈O.01),与PCO2呈负相关(P〈O.01),CD59分布的变化与CD55变化类似。结论:氧分压和环境温度过低、二氧化碳分压过高都是诱发免疫活性细胞激活的有效因素。此环境暴露对血细胞自身保护作用有随时间累积的效应。 相似文献
2.
CD55 and CD59 are glycosylphosphatidylinositol-anchored proteins with complement inhibitory properties. CD55 inhibits the formation of C3 convertases, and CD59 prevents the terminal polymerisation of the membrane attack complex. It has been reported that SLE patients seems to have an acquired deficiency of these proteins associated with secondary autoimmune haemolytic anaemia and lymphopenia. The aim of this study was to evaluate the presence of altered CD55 and CD59 expression on peripheral blood cells from SLE patients. Flow cytometric analyses were performed on red and white blood cells from 23 SLE patients and 23 healthy controls. We observed more CD55- and CD59-lymphocytes (p = 0.005 and p = 0.019, respectively), and CD59-granulocytes (p = 0.045) in SLE patients than in controls. These results suggest there is an altered pattern of CD55 and CD59 expression on the peripheral blood cells of SLE patients, and it may play a role in the cytopenias in these patients. 相似文献
3.
Bilyy R Kit Y Hellman U Tryndyak V Kaminskyy V Stoika R 《Cell biology international》2005,29(11):920-928
We recently established that an increased expression of alpha-D-mannose (Man)- and beta-D-galactose-rich plasma membrane glycoproteins (GPs) is characteristic for apoptotic cells in vitro [Bilyy, R.O., Stoika, R.S., 2003. Lectinocytochemical detection of apoptotic murine leukemia L1210 cells. Cytometry 56A, 89-95]. It was independent of cell line or apoptosis-inducing agent, and can therefore be considered as a selective marker for identification and isolation of apoptotic cells [Bilyy, R.O., Antonyuk, V.O., Stoika, R.S., 2004. Cytochemical study of role of alpha-D-mannose- and beta-D-galactose-containing glycoproteins in apoptosis. J. Mol. Histol. 35, 829-838]. The main goals of the present study were: (1) to determine whether an increased expression of specific GPs also takes place after apoptosis induction in vivo; and (2) to identify additional characteristics of the membrane GP markers of the apoptotic cells. To reach these goals, we studied the expression of alpha-Man-rich membrane GPs in murine leukemia L1210 cells inoculated into abdominal cavities of mice which were then subjected to the action of apoptosis inducer doxorubicin. Another experimental model used in the present work was splenocytes obtained from mice treated with dexamethasone. Lectin-affinity chromatography and PAGE electrophoresis, or PAGE electrophoresis and lectinoblot analysis were applied for isolation of plasma membrane GPs (34 kDa, and high M(W) of approximately 600 and 800 kDa) whose expressions were increased during apoptosis. Triton X-114 treatment of cell membrane samples showed that the apoptotic cell-specific GPs were localized in the peripheral and integral compartments of plasma membrane. Apoptosis in vitro and in vivo was accompanied by an increased expression of the same GP, identified by MALDI-TOF MS analysis as the microtubule-actin cross-linking factor 1. Other GPs, whose expressions were also increased at apoptosis, were similarly identified as G-protein beta-subunit like (Acc# BAA06185.1) and dystonin isoform beta. 相似文献
4.
Experimental autoimmune thyroiditis (EAT), a model for Hashimoto's thyroiditis, is a T cell-mediated disease inducible with mouse thyroglobulin (mTg). Pretreatment with mTg, however, can induce CD4+ T cell-mediated tolerance to EAT. We demonstrate that CD4+CD25+ regulatory cells are critical for the tolerance induction, as in vivo depletion of CD25+ cells abrogated established tolerance, and CD4+CD25+ cells from tolerized mice suppressed mTg-responsive cells in vitro. Importantly, administration of an agonistic CD137 monoclonal antibody (mAb) inhibited tolerance development, and the mediation of established tolerance. CD137 mAb also inhibited the suppression of mTg-responsive cells by CD4+CD25+ cells in vitro. Signaling through CD137 likely resulted in enhancement of the responding inflammatory T cells, as anti-CD137 did not enable CD4+CD25+ T cells to proliferate in response to mTg in vitro. 相似文献
5.
Taatjes DJ Wadsworth MP Zaman AK Schneider DJ Sobel BE 《Histochemistry and cell biology》2007,128(3):275-283
Confocal scanning laser microscopy was used to investigate the myocardium of control C57BL/6 and plasminogen activator inhibitor
1 knockout (PAI-1KO) mice 3 days following persistent ligation of the left descending coronary artery. Paraffin sections taken
from infarcted areas of the left ventricle were stained with antibodies recognizing cardiomyocytes, neutrophils, macrophages
and apoptotic cells. In both animal groups, a strong neutrophil response was noted in the infarcted myocardium, with a large
proportion of these cells also displaying staining for anti-α-sarcomeric actin in the PAI-1KO animals. Abundant macrophages
were also identified in the infarcted regions of both animal groups, forming demonstrable streams at the border region in
the C57BL/6 control animals. Surprisingly, only sparse cells from both animal groups were labeled with the apoptotic markers
anti-cleaved caspase 3 antibody and anti-single stranded DNA antibody (following formamide treatment). A dual immunostaining
protocol was developed to localize both of these apoptotic markers in the same cell. Again, only scattered cells were found
displaying both markers in the zones of infarction, suggesting that 3 days of persistent ischemia results in a robust necrotic
response, but only a very minor apoptotic response in this mouse model. 相似文献
6.
Release of iC3b from apoptotic tumor cells induces tolerance by binding to immature dendritic cells in vitro and in vivo 总被引:2,自引:0,他引:2
Chemo- as well as immunotherapeutical approaches induce apoptosis in tumor cells. Apoptotic cells are known to activate homologous
complement and to be opsonized with iC3b. Since maturation of dendritic cells (DC) can be inhibited by binding of iC3b to
the complement receptor 3 (CR3, CD11b/CD18) and because immature DC induce tolerance, we investigated the induction of tolerance
after pulsing DC with apoptotic cells in the presence or absence of native serum. Apoptosis in pancreatic carcinoma cells
was induced either by heat-stress, chemotherapy or anti-Her2 antibody. Monocyte-derived DC were pulsed with apoptotic cells
with or without native serum. DC were analyzed for the maturation state by flow cytometry and the cytotoxic activity was determined.
Tolerance was prevented by addition of substances such as anti CD11b or N–acetyl-D-Glucosamine (NADG) which block iC3b binding
to CR3. Furthermore, binding of iC3b from apoptotic cells to DC was blocked in a syngeneic pancreatic carcinoma mouse model.
All of the former strategies for apoptosis induction resulted in iC3b release. Pulsing DC with apoptotic cells in the presence
of serum prevents maturation of DC and induces finally tolerance. This tolerance could be prevented almost completely by blocking
the interaction of iC3b with the CR3 receptor. This could be shown as well in an immunocompetent mouse model. Chemo- as well
as immunotherapeutical approaches induce apoptosis in tumor cells. Release of iC3b from apoptotic tumor cells prevents fully
maturation of DC and immature DC induce antigen-specific silencing or tolerance. Blocking of iC3b-binding could mostly prevent
this effect. 相似文献
7.
Takemi Oguma Takeshi Ono Toshimitsu Kajiwara Yasushi Miyahira Yasuo Yoshihara 《Cellular immunology》2009,260(1):21-3567
When the CD4+CD8+ thymic lymphoma cells were treated with puromycin, we found that most of the cells died at 0.3-1 μg/ml of puromycin within 24 h. However, cell death was greatly reduced when the dose of puromycin was increased. Similar dose-pattern of cell death was observed in thymocytes and the sensitivity to puromycin was greater in CD4+CD8+ thymocytes than CD4+CD8− thymocytes. The induction of apoptosis was blocked by the protein synthesis inhibitor cycloheximide, and to some extent by transfection of Bcl-xL or Bcl-2 genes. Expression of GRP78 was up-regulated after treatment with a small dose of puromycin, and the cell death by puromycin was blocked in the presence of caspase 12 inhibitor. These results indicated that the induction of cell death by low-dose puromycin was due to endoplasmic reticulum stress. Furthermore, we found that dexamethasone, a synthetic glucocorticoid, and puromycin worked synergistically to induce cell death in thymocytes. 相似文献
8.
Hemopoiesis in orthopteran insects occurs in a hemopoietic organ that is located bilaterally along the aorta. This organ is also known as a reticulo-hemopoietic organ because of the rich presence of reticular cells. This study was performed to further elucidate hemopoiesis in the reticulo-hemopoietic organ of an orthopteran, Euprepocnemis shirakii. We focused on the question why reticular cells are so abundant (35% of cells in hemopoietic organ). Interestingly, 21% of these reticular cells surrounded hemocytes with their reticular cytoplasm. The surrounded hemocytes were distinguished by their different size and darkly stained nucleus. These cells were characterized by immunostaining using antibodies against several types of hemocytes: 45% of the surrounded hemocytes were CD34+, and these positive cells were double stained (over 85%) when immunostained by another hemopoietic pluripotent cell marker, Sca-1. Transmission electron microscopic analysis showed that reticular cells surrounded hemocytes containing large nuclei and poorly developed cytoplasmic organelles. This strongly suggests that the reticular cells surround hemopoietic stem cells. Additionally, surrounded hemopoietic progenitor cells are undergoing apoptosis as indicated by the TUNEL assay. The enclosed apoptotic cells are engulfed and then phagocytosed by reticular cells. Our results suggest that reticular cells are related to the differentiation and apoptosis of hemopoietic stem cells. 相似文献
9.
Kuraishi T Manaka J Kono M Ishii H Yamamoto N Koizumi K Shiratsuchi A Lee BL Higashida H Nakanishi Y 《Experimental cell research》2007,313(3):500-510
Apoptotic cell phagocytosis is initiated through the specific interaction between markers for phagocytosis present at the surface of targets and their receptors of phagocytes. Although many molecules have been proposed to be phagocytosis markers and receptors in mammals, information as to the identity of those molecules is limited for invertebrate animals. Calreticulin, a molecular chaperone that functions in the lumen of the endoplasmic reticulum, was recently reported to be the second general marker, the membrane phospholipid phosphatidylserine being the first, for mammalian apoptotic cells to be recognized by phagocytes. We here asked whether or not calreticulin serves as a marker for phagocytosis in Drosophila. Phagocytosis of apoptotic S2 cells by Drosophila hemocyte-derived l(2)mbn cells, which we previously showed to occur independent of phosphatidylserine, was inhibited by the addition of anti-calreticulin antibody. This inhibition was observed when the target cells, but not phagocytes, were pre-incubated with the antibody. In addition, RNA interference-mediated reduction of calreticulin expression in apoptotic S2 cells, but not in l(2)mbn cells, reduced the level of phagocytosis. An immunocytochemical analysis revealed that calreticulin is widely distributed at the surface of viable S2 cells. After the induction of apoptosis, cell surface calreticulin seemed to form aggregates, with no change in its amount. Furthermore, in embryos of a mutant Drosophila strain that expresses calreticulin at a reduced level, the level of phagocytosis of apoptotic cells was about a half of that observed in embryos of a wild-type strain. These results collectively indicate that calreticulin is the first molecule to be identified as a marker for phagocytosis of apoptotic cells by Drosophila phagocytes. 相似文献
10.
Stieglmaier J Bremer E Kellner C Liebig TM ten Cate B Peipp M Schulze-Koops H Pfeiffer M Bühring HJ Greil J Oduncu F Emmerich B Fey GH Helfrich W 《Cancer immunology, immunotherapy : CII》2008,57(2):233-246
Although the treatment outcome of lymphoid malignancies has improved in recent years by the introduction of transplantation
and antibody-based therapeutics, relapse remains a major problem. Therefore, new therapeutic options are urgently needed.
One promising approach is the selective activation of apoptosis in tumor cells by the tumor necrosis factor-related apoptosis-inducing
ligand (TRAIL). This study investigated the pro-apoptotic potential of a novel TRAIL fusion protein designated scFvCD19:sTRAIL,
consisting of a CD19-specific single-chain Fv antibody fragment (scFv) fused to the soluble extracellular domain of TRAIL
(sTRAIL). Potent apoptosis was induced by scFvCD19:sTRAIL in several CD19-positive tumor cell lines, whereas normal blood
cells remained unaffected. In mixed culture experiments, selective binding of scFvCD19:sTRAIL to CD19-positive cells resulted
in strong induction of apoptosis in CD19-negative bystander tumor cells. Simultaneous treatment of CD19-positive cell lines
with scFvCD19:sTRAIL and valproic acid (VPA) or Cyclosporin A induced strongly synergistic apoptosis. Treatment of patient-derived
acute B-lymphoblastic leukemia (B-ALL) and chronic B-lymphocytic leukemia (B-CLL) cells resulted in strong tumoricidal activity
that was further enhanced by combination with VPA. In addition, scFvCD19:sTRAIL prevented engraftment of human Nalm-6 cells
in xenotransplanted NOD/Scid mice. The pre-clinical data presented here warrant further investigation of scFvCD19:sTRAIL as
a potential new therapeutic agent for CD19-positive B-lineage malignancies.
This work was supported by Schickedanz KinderKrebs Stiftung (JS) and grants from the Association “Kaminkehrer helfen krebskranken
Kindern” (CK, GHF), the Association of supporters of the University of Erlangen Childrens’s Hospital (GHF) and the Dutch Cancer
Society (RUG 2002-2668 and 2005-3358) (EB, BC, WH).
Julia Stieglmaier and Edwin Bremer contributed equally. 相似文献
11.
To avoid destruction by complement, normal and malignant cells express membrane glycoproteins that restrict complement activity.
These include decay-accelerating factor (DAF, CD55), membrane cofactor protein (MCP, CD46) and protectin (CD59), which are
all expressed on colonic adenocarcinoma cells in situ. In this study we have characterised the C3/C5 convertase regulators
DAF and MCP on the human colonic adenocarcinoma cell line HT29. DAF was found to be a glycosyl-phosphatidylinositol-anchored
70-kDa glycoprotein. Blocking experiments with F(ab′)2 fragments of the anti-DAF monoclonal antibody BRIC 216 showed that DAF modulates the degree of C3 deposition and mediates
resistance to complement-mediated killing of the cells. The expression and function of DAF were enhanced by tumour necrosis
factor α (TNFα) and interleukin-1β (IL-1β). Cells incubated with interferon γ (IFNγ) did not alter their DAF expression. Two
MCP forms were expressed, with molecular masses of approximately 58 kDa and 68 kDa, the lower form predominating. MCP expression
was up-regulated by IL-1β, but not by TNFα or IFNγ. Expression of DAF and MCP promotes resistance of colonic adenocarcinoma
cells to complement-mediated damage, and represents a possible mechanism of tumour escape.
Received: 18 July 1995 / Accepted: 4 January 1996 相似文献
12.
Sato K Tateishi S Kubo K Mimura T Yamamoto K Kanda H 《Biochemical and biophysical research communications》2005,330(1):226-232
CD25(+)CD4(+) regulatory T cells suppress immune responses and are believed to play roles in preventing autoimmune diseases. However, the mechanism(s) underlying the suppression and the regulation of their homeostasis remain to be elucidated. Here we show that these regulatory T cells downregulated CD25(-)CD4(+) T-cell-mediated production of IL-12 from antigen-presenting cells, which can act as a growth factor for CD25(-)CD4(+) T cells. We further found that CD25(+)CD4(+) T cells, despite their well-documented "anergic" nature, proliferate significantly in vitro only when CD25(-)CD4(+) T cells are present. Notably, this proliferation was strongly dependent on IL-2 and relatively independent of IL-12. Thus, CD25(+)CD4(+) T cells suppress CD25(-)CD4(+) T-cell responses, at least in part, by inhibiting IL-12 production while they themselves can undergo proliferation with the mediation of CD25(-)CD4(+) T cells in vitro. These results offer a novel negative feedback system involving a tripartite interaction among CD25(+)CD4(+) and CD25(-)CD4(+) T cells, and APCs that may contribute to the termination of immune responses. 相似文献
13.
Py B Bouchet J Jacquot G Sol-Foulon N Basmaciogullari S Schwartz O Biard-Piechaczyk M Benichou S 《Apoptosis : an international journal on programmed cell death》2007,12(10):1879-1892
In addition to its positive signaling function in the antigen presentation process, CD4 acts as the primary receptor for HIV-1.
Contact between CD4 and the viral envelope leads to virus entry, but can also trigger apoptosis of uninfected CD4+ T-cells through a mechanism that is poorly understood. We show that Siva-1, a death domain-containing proapoptotic protein,
associates with the cytoplasmic domain of CD4. This interaction is mediated by the cysteine-rich region found in the C-terminal
part of the Siva-1 protein. Expression of Siva-1 specifically increases the susceptibility of both T-cell lines and unstimulated
human primary CD4+ T-lymphocytes to CD4-mediated apoptosis triggered by the HIV-1 envelope, and results in activation of a caspase-dependent
mitochondrial pathway. The same susceptibility is observed in T-cells expressing a truncated form of CD4 that is able to recruit
Siva-1 but fails to associate with p56Lck, indicating that Siva-1 participates in a pathway independent of the p56Lck kinase activity. Altogether, these results suggest that Siva-1 might participate in the CD4-initiated signaling apoptotic
pathway induced by the HIV-1 envelope in T-lymphoid cells.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
14.
15.
血小板生成素诱导胎肝CD34~ 造血干/祖细胞增殖分化与周期蛋白表达的关系 总被引:1,自引:0,他引:1
为了解胚胎时期巨核细胞增殖分化特有的内在机制 ,本研究观察了在体外培养体系中 ,胎肝源CD3 4 造血干 /祖细胞在血小板生成素 (thrombopoietin ,TPO)作用下增殖分化特征与相关周期蛋白B1、D1和D3表达及细胞内水平变化的关系。结果发现 :( 1)经 12d培养后 ,TPO使胎肝源CD3 4 细胞数从 1× 0 5个细胞 /ml增加到 13 12± 4 0 6× 10 5个细胞 /ml,CD4 1 细胞增加到了 95 % ,CD3 4 细胞下降到了 3 % ,大部分细胞的DNA倍性为 2N ,少数为 4N ,无大于 4N巨核细胞 ,TPO对MegaCultTm C胶原半固体培养体系中胎肝源CD3 4 细胞形成CFU Mk集落产率的影响呈明显的剂量效应关系 ;( 2 )在整个培养期间 ,周期蛋白B1表达逐渐增加 ,并保持在一个高水平上 ,培养后期 ,高水平的周期蛋白B1出现在G1期细胞上 ;( 3 )周期蛋白D1和D3表达先增加 ,培养后期细胞内水平下降 ,且以G2期细胞为主。该结果提示 :( 1)TPO通过上调周期蛋白B1和在所有细胞周期时限上调周期蛋白D1和D3表达 ,促进巨核细胞祖细胞的增殖分化 ;( 2 )周期蛋白B1在G2 M期的持续高水平和周期蛋白D1和D3在G2 M期的水平下降 ,可能导致胎肝源巨核细胞核内有丝分裂延迟或阻滞。 相似文献
16.
Hennersdorf F Florian S Jakob A Baumgärtner K Sonneck K Nordheim A Biedermann T Valent P Bühring HJ 《Cell research》2005,15(5):325-335
INTRODUCTIONBasophils and mast cells are important effector cells ofinflammatory reactions [1-3]. In contrast to eosinophilsand neutrophils, they possess high-affinity immunoglo-bulin (Ig) E receptors (FcεRI) that are cross-linked uponengagement of recep… 相似文献
17.
Involvement of catalase in the apoptotic mechanism induced by apigenin in HepG2 human hepatoma cells
Valdameri G Trombetta-Lima M Worfel PR Pires AR Martinez GR Noleto GR Cadena SM Sogayar MC Winnischofer SM Rocha ME 《Chemico-biological interactions》2011,(2):180-189
Apigenin has been reported to inhibit proliferation of cancer cells; however, the mechanism underlying its action is not completely understood. Here, we evaluated the effects of apigenin on the levels of expression and activity of antioxidant enzymes, and the involvement of ROS in the mechanism of cell death induced by apigenin in HepG2 human hepatoma cells. Upon treatment with apigenin, HepG2 cells displayed a reduction in cell viability in a dose- and time-dependent manner, and some morphological changes. In addition, apigenin treatment induced ROS generation and significantly decreased the mRNA levels and activity of catalase and levels of intracellular GSH. On the other hand, apigenin treatment did not alter the expression or activity levels of other antioxidant enzymes. Addition of exogenous catalase significantly reduced the effects of apigenin on HepG2 cell death. We also demonstrated that HepG2 cells are more sensitive to apigenin-mediated cell death than are primary cultures of mouse hepatocytes, suggesting a differential toxic effect of this agent in tumor cells. Our results suggest that apigenin-induced apoptosis in HepG2 cells may be mediated by a H2O2-dependent pathway via reduction of the antioxidant defenses. 相似文献
18.
Kevin B. Strychar Mike Coates Terrence J. Piva 《Journal of experimental marine biology and ecology》2004,304(1):99-121
The study of symbiont cells lost from bleached scleractinian corals Acropora hyacinthus, Favites complanata, and Porites solida and octocorals Sarcophyton ehrenbergi, Sinularia sp., and Xenia sp. using flow cytometry shows that Symbiodinium die from either apoptosis or necrosis. Despite the majority of lost Symbiodinium cells being viable at 28 °C, the predominance of apoptotic and necrotic symbiont cells at higher temperatures indicates that the proportion of live cells decreases with increasing temperature. This implies that reinfection of corals at high temperatures by Symbiodinium lost from scleractinian corals may be less frequent than previously described, since many of the symbiont cells exhibit nonreversible symptoms of approaching cell death. The fraction of viable Symbiodinium cells lost from S. ehrenbergi, Xenia sp., and Sinularia at 32 °C was greater than that at 28 °C. At 34 °C, the fraction of viable cells lost from S. ehrenbergi and Xenia sp. fell but not from Sinularia sp., which suggests that their symbionts have higher temperature tolerances. Thus, Symbiodinium from octocorals may represent “pools” of genetically resistant symbionts available for reinfection of other reef organisms. This has been proposed previously for Symbiodinium in some scleractinian corals, but this is the first evidence for such, particularly for an octocoral. Many of the viable cells, determined using Trypan blue staining techniques, are in fact actually undergoing apoptosis or necrosis, when examined using Annexin V-fluor and propidium iodide staining profiles. The characterization of more apoptotic and necrotic cells than viable cells is critical, as this indicates that the loss of Symbiodinium cells cannot be beneficial to other bleached corals for symbiotic reassociation. 相似文献
19.
Tao Tu Chunxia Zhang Huiwen Yan Yongting Luo Ruirui Kong Pushuai Wen Zhongde Ye Jianan Chen Jing Feng Feng Liu Jane Y Wu Xiyun Yan 《Cell research》2015,25(3):275-287
Angiogenesis, a process that newly-formed blood vessels sprout from pre-existing ones, is vital for vertebrate development and adult homeostasis. Previous studies have demonstrated that the neuronal guidance molecule netrin-1 participates in angiogenesis and morphogenesis of the vascular system. Netrin-1 exhibits dual activities in angiogenesis: either promoting or inhibiting angiogenesis. The anti-angiogenic activity of netrin-1 is mediated by UNC5B receptor. However, how netrin-1 promotes angiogenesis remained unclear. Here we report that CD146, an endothelial transmembrane protein of the immunoglobulin superfamily, is a receptor for netrin-1. Netrin-1 binds to CD146 with high affinity, inducing endothelial cell activation and downstream signaling in a CD146-dependent manner. Conditional knockout of the cd146 gene in the murine endothelium or disruption of netrin-CD146 interaction by a specific anti-CD146 antibody blocks or reduces netrin-1-induced angiogenesis. In zebrafish embryos, downregulating either netrin-1a or CD146 results in vascular defects with striking similarity. Moreover, knocking down CD146 blocks ectopic vascular sprouting induced by netrin-1 overexpression. Together, our data uncover CD146 as a previously unknown receptor for netrin-1 and also reveal a functional ligand for CD146 in angiogenesis, demonstrating the involvement of netrin-CD146 signaling in angiogenesis during vertebrate development. 相似文献
20.
Tyrosine phosphorylation of a novel 100-kDa protein coupled to CD28 in resting human T cells is enhanced by a signal through TCR/CD3 complex 总被引:1,自引:0,他引:1
Matsumoto A Dobashi H Ohnishi H Tanaka T Kubota Y Kitanaka A Ishida H Tokuda M Waki M Kubo A Ishida T 《Microbiology and immunology》2003,47(1):63-69
For T cell activation, two signals are required, i.e., a T cell receptor (TCR)/CD3-mediated main signal and a CD28-mediated costimulatory signal. CD28 binds to its ligand (CD80 or CD86) and transduces the most important costimulatory signal. The cytoplasmic domain of the CD28 molecule, composed of 41 amino acids, does not contain any intrinsic enzyme activity. The cytoplasmic domain of CD28 is remarkably conserved among species and is associated with a number of signaling molecules that affect the main signal. We report here that a tyrosine phosphorylated 100-kDa protein (ppl00) was coupled to the CD28 cytoplasmic domain in Jurkat and human peripheral T cells. The pp100 was distinguished from other CD28 associated molecules such as Vav, STAT5, PI 3-kinase, Valosin-containing protein (VCP), Nucleolin, Gab2 (Grb2-associated binding protein 2), and STAT6. The tyrosine phosphorylation of pp100 coprecipitated with CD28 was enhanced by CD3 stimulation by the specific antibody, tyrosine phosphatase inhibitor and PKC activator. Tyrosine phosphorylation of pp100 was attenuated by the prior addition of PKC inhibitor. These findings indicate that pp100 is a novel tyrosine phosphorylated protein coupled to CD28 under continuous control of tyrosine phosphatases and might play a role in T cell activation augmented by a TCR/CD3-mediated main signal. 相似文献