AIT of 3-day established i.d. MCA-205 tumors, T cells from D9 vs D12...
FIGURE 2. AIT of 3-day established i.d. MCA-205 tumors, T cells from D9 vs D12 TDLN compared. Syngeneic B6 mice were injected intra fl ank with 1.5 ? 10 6 MCA-205 cells as in Fig. 1 to synchronously prepare D9 and D12 TDLN UnF and L-selectin low T cell groups. Following 5-day culture activation, individual groups were harvested and administered to B6 mice with 3-day established i.d. tumors. The treatment groups (10 mice per group, except group B ? 5 mice) were as follows: A , No T B , L-selectin low T cells (5 ? 10 6 ) from D9 TDLN (D9 L -sel(low) 5E6); C , UnF T cells (25 ? 10 6 ) from D9
ContextTDLN T cells harvested from mice bearing weakly immunogenic tumors contained a minor ( ? 15%) subpopulation of L-selectin low T cells. When this fraction was isolated from either day 9 (D9) or D12 TDLN, and then culture activated and adoptively transferred into syngeneic mice, 5 ? 10 6 L-selectin low T cells consistently cured recipient mice bearing 3-day established pulmonary, intra-
cranial, and i.d. tumors (see below and Refs. 11 and 14). As reported previously, cure following such AIT was antigenically restricted to the tumor used for TDLN sensitization and required intratumoral T cell in fi ltration (8 – 11, 13). Furthermore, no adjunct treatment such as rIL-2 was necessary for cure (11). In contrast to isolated L-selectin low T cells, which were therapeutically effective whether obtained from D9 or D12 TDLN, a marked therapeutic disparity was observed when we compared the potentials of UnF T cells from D9 TDLN to those from D12 TDLN in treating established i.d. tumors. Culture activation and adoptive transfer of even 100 ? 10 6 UnF T cells from D12 TDLN resulted in survival prolongation but almost invariably failed to prevent lethal i.d. tumor progression (Figs. 1 and 2). In contrast, as few as 25 ? 10 6 culture-activated UnF T cells from D9 TDLN were consistently as ef fi cient as 5 ? 10 6 puri fi ed D9 or D12 L-selectin low T cells for achieving i.d. tumor rejection (Fig. 2). This striking therapeutic disparity was observed for both CT-26 and MCA-205 i.d. tumors in syngeneic BALB/c and B6 mice, respectively, indicating that this phenomenon was not restricted to a single tumor model or mouse strain (Figs. 1 and 2). Because UnF T cells culture activated from D12 TDLN provided effective AIT for both established pulmonary and intracranial tumors in previous experiments, their ineffectiveness against i.d. tumors compared with UnF T cells from D9 TDLN was un- anticipated (8 – 11, 14). We sought to authenticate this therapeutic incongruity by performing AIT against simultaneous 3-day challenges of i.d., intracranial, and pulmonary tumors. Without AIT, triply challenged mice died of visceral tumor by day 25 of challenge, with progressive i.d. tumors also evident (Fig. 3). Mice treated with 5 ? 10 6 L-selectin low or 50 ? 10 6 UnF T cells culture activated from D9 TDLN were cured of all three challenges, as were mice treated with 5 ? 10 6 L-selectin low T cells from D12 TDLN (Fig. 3). In contrast, mice treated with 50 ? 10 6 UnF T cells culture activated from D12 TDLNJoin ResearchGate to access over 30 million figures and 100+ million publications – all in one place.Published inDec 2002The Journal of Immunology[...]Existuje mo?nost deplece Treg buněk in vivo bez rizika indukce autoimunitní odpovědi? Z my?ích model? vypl?vá, ?e k indukci tumor specifick?ch Treg buněk dochází velmi ?asně ve v?voji nádoru [59]. Tento fakt m??e mít zna?n? klinick? v?znam , nebo? k indukci Treg buněk dojde pravděpodobně p?ed stanovením diagnózy nádoru u vět?iny pa cient?. ABSTRACT: Regulatory T-lymphocytes (Treg) are essential for regulation of immune homeostasis and prevention of autoimmune disease development. Regulatory T-cells prevent the onset of they keep immune homeostasis and modulate immune response during infection. Their activity is precisely controlled. Regulatory T-cells belong to one group of immune cells, which can support tumor survival and growth. They realize their function through inhibition of effector T-cells and by regulation of tumor microenvironment through production of various soluble factors. Many publications have proven that the amount of Treg cells is elevated in both solid tumors and in hematologic malignancies. Nevertheless, little is known about mechanisms, which allow increase and maintenance of elevated Treg cells in cancer patients. In this review, we will focus, among others, on the description of function and phenotype of Treg cells, their modulation of humoral immune response and interaction with cancer stem cells. Current development of modern tumor immunotherapy allows new possibilities of influencing Treg cells function.Key words: regulatory T-cells - Foxp3 - phenotype - humoral immunity - cancer stem cellsThis work was supported by project VaVpI RECAMO - CZ.1.05/2.1.00/03.010.The author declares he has no potential conflicts of interest concerning drugs, products, or services used in the study.The Editorial Board declares that the manuscript met the ICMJE recommendation for biomedical papers.Submitted: 2. 9. 2015Accepted: 10. 11. 2015. Full-text · Article · Dec 2015 The development of T Reg cells during tumour progression has been addressed in several model systems. For example, T Reg development in a fibrosarcoma model in C57BL/6N mice as well as in a colon adenocarcinoma model in BALB/c mice has been shown to have lethal tumour progression [147]. The T Reg cells during tumour development have been shown to have high suppressor capacity. ABSTRACT: Since the formulation of the tumour immunosurveillance theory, considerable focus has been on enhancing the effectiveness of host antitumour immunity, particularly with respect to T cells. A cancer evades or alters the host immune response by various ways to ensure its development and survival. These include modifications of the immune cell metabolism and T cell signaling. An inhibitory cytokine milieu in the tumour microenvironment also leads to immune suppression and tumour progression within a host. This review traces the development in the field and attempts to summarize the hurdles that the approach of adoptive T cell immunotherapy against cancer faces, and discusses the conditions that must be improved to allow effective eradication of cancer.
Copyright (C) 2015 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.Article · Jun 2015 Tregs are cells involved in the control of self-tolerance and immune homeostasis, with suppressive capabilities. These cells are early induced during tumor development and are shown to contribute to tumor tolerance [95, 96]. The presence of Tregs in tumors is associated with a poor prognosis [97]. ABSTRACT: Multiple myeloma (MM) is a hematologic malignancy of differentiated plasma cells that accumulates and proliferates in the bone marrow. MM patients often develop bone disease that results in severe bone pain, osteolytic lesions, and pathologic fractures. These skeletal complications have not only a negative impact on quality of life but also a possible effect in overall survival. MM osteolytic bone lesions arise from the altered bone remodeling due to both increased osteoclast activation and decreased osteoblast differentiation. A dysregulated production of numerous cytokines that can contribute to the uncoupling of bone cell activity is well documented in the bone marrow microenvironment of MM patients. These molecules are produced not only by malignant plasma cells, that directly contribute to MM bone disease, but also by bone, immune, and stromal cells interacting with each other in the bone microenvironment. This review focuses on the current knowledge of MM bone disease biology, with particular regard on the role of bone and immune cells in producing cytokines critical for malignant plasma cell proliferation as well as in osteolysis development. Therefore, the understanding of MM pathogenesis could be useful to the discovery of novel agents that will be able to both restore bone remodelling and reduce tumor burden. Full-text · Article · May 2013 The development of T R cells during tumor progression has been addressed in a several model systems. For example, T R development in a fibrosarcoma model in C57BL/6N mice as well as in a colon adenocarcinoma model in BALB/c mice has been shown to have lethal tumor progression [7]. The T R cells during tumor development have shown to have high suppressor capacity. ABSTRACT: Prostate Cancer (PCa) is the most common non-skin malignancy and commonly diagnosed cancer, and second most cancer responsible for death in men in United States. Prior studies in animal models of PCa as well as in human, demonstrated that the prostate produces several growth factors. Addition or blocking of these growth factors can alter the PCa cell proliferation and other important functions. Among these growth factors, transforming growth factor-β1 (TGF-β) plays significant role in tumorigenicity, displays potent immunosuppressive activities, and is required for the conversion of conventional CD4 + T cells to Foxp3 + regulatory T cells (T R). T R that expresses the transcription factor Foxp3 is essential for normal immune function. Absence of T R cells results in multi-organ autoimmunity and death. This chapter reviews the underlying mechanisms involved in the context of TGF-β and/or T R in prostate cancer development and clearance. Full-text · Article · Jan 2013 · Clinical and Developmental Immunology +1 more author...Naturally occurring and adaptive regulatory T cells (Tregs) are anergic cells with suppressive capabilities that constitute 5–10% of CD4 cells. These cells are induced early during tumor development and were shown to contribute to tumor tolerance [46] [47]. ABSTRACT: Multiple myeloma (MM) is a life-threatening haematological malignancy for which standard therapy is inadequate. Autologous stem cell transplantation is a relatively effective treatment, but residual malignant sites may cause relapse. Allogeneic transplantation may result in durable responses due to antitumour immunity mediated by donor lymphocytes. However, morbidity and mortality related to graft-versus-host disease remain a challenge. Recent advances in understanding the interaction between the immune system of the patient and the malignant cells are influencing the design of clinically more efficient study protocols for MM.
Cellular immunotherapy using specific antigen-presenting cells (APCs), to overcome aspects of immune incompetence in MM patients, has received great attention, and numerous clinical trials have evaluated the potential for dendritic cell (DC) vaccines as a novel immunotherapeutic approach. This paper will summarize the data investigating aspects of immunity concerning MM, immunotherapy for patients with MM, and strategies, on the way, to target the plasma cell more selectively. We also include the MM antigens and their specific antibodies that are of potential use for MM humoral immunotherapy, because they have demonstrated the most promising preclinical results. Full-text · Article · May 2012 Preclinical studies in rat and murine glioma models first demonstrated that polyclonal, glioma-specific T cells could eradicate CNS gliomas (Baldwin et al., 1997; Kruse et al., 1990; Plautz et al., 1997; Rice et al., 1997 ) and was associated with enhanced trafficking of these lymphocytes to the brain (Hazelrigg et al., 2002). Subsequent work demonstrated that the draining LN population, from which these lymphocytes are isolated, also includes suppressor populations that can impair the efficacy of the adoptively transferred population (Peng et al., 2002). Removal of the CD62L high population enriched the lymphocyte population with enhanced antitumor activity (Plautz et al., 1997). ABSTRACT: T-cell mediated immunotherapy is a conceptually attractive treatment option to envisage for glioma, since T lymphocytes can
actively seek out neoplastic cells in the brain, and they have the potential to safely and specifically eliminate tumor. Some
antigenic targets on glioma cells are already defined, and we can be optimistic that more will be discovered from progress
in T-cell epitope identification and gene expression profiling of brain tumors. In parallel, advances in immunology (regional
immunology, neuroimmunology, tumor immunology) now equip us to build upon the results from current immunotherapy trials in
which the safety and feasibility of brain tumor immunotherapy have already been confirmed. We can now look to the next phase
of immunotherapy, in which we must harness the most promising basic science advances and existing clinical expertise, and
apply these to randomized clinical trials to determine the real clinical impact and applicability of these approaches for
treating patients with currently incurable malignant brain tumors.Chapter · Jan 2009 · Clinical and Developmental ImmunologyA/I主流级CPU PK：锐龙3 1300X VS 酷睿i3 6100_凤凰科技
A/I主流级CPU PK：锐龙3 1300X VS 酷睿i3 6100
用微信扫描二维码分享至好友和朋友圈
原标题：A/I主流级CPU PK：锐龙3 1300X VS 酷睿i3 6100 　　曾经有如“一滩死
原标题：A/I主流级CPU PK：锐龙3 1300X VS 酷睿i3 6100
　　曾经有如“一滩死水”般的CPU市场能够在今年重获生机，多亏了AMD在今年推出的“锐龙”系列CPU。正是因为AMD锐龙的到来，并在半年内迅速完成从千元内入门级到数千元骨灰级的布局，我们才能看到数年来一直主导CPU市场的Intel，迫于压力拿出了四核起步、6核封顶的第八代酷睿。
　　能够迫使Intel放弃原定计划，提前拿出第八代酷睿抗衡AMD的凌厉攻势，足以证明锐龙系列CPU的成功。当然了，锐龙系列处理器能够收获成功，也离不开相比同级别第七代酷睿处理器更高一级的规格与更优秀的性能，即便是千元内的入门级锐龙，也都是地地道道的“真四核”CPU。
　　可以说锐龙的成功是离不开广大用户的，今天随着锐龙全系列的力战各个产品线，我们的本次的也关注更多更加基层的使用群体。我们知道用户痴迷于强力性能的高性能品质，但对于三四线城市的主流用户来说，性价比以及入门级别的处理器才是打动他们的核心驱动力。因此我们针对广大三四线城市用户带来他们非常在意的入门级别强力对比评测，AMD锐龙3 1300X 与 酷睿 i3 6100这两款千元级别产品就是时下三四线城市用户非常推崇的， 但是选择方面用户不是十分明确，今天我们特地带来的专项评测下面大家慢慢细品。
首先让我们来分析一下两款CPU的情况：
　　AMD锐龙3 1300X处理器：主频3.5G，睿频3.7G，4核心4线程，为不锁倍频设计，可以说四核毕竟是4核一寸长一寸强，从后面的测玩家就会慢慢了解了，可以说锐龙3 1300X性价比较好。同时其可以做到不锁倍频，把可玩空间留给玩家，让玩家通过自己动手调节的方式获得更大的性能提升，熟练的玩家可以做到15秒瞬间超频，在超频的自由性、灵活性上AMD一贯做的比Intel要好。
　　对比INTEL Core i3-6100，锐龙CPU还是非常有竞争优势的！不论是价格还是性能，目前锐龙3 1300X价格在889，INTEL i3-6100也在800左右，但是性能可不是几十元能弥补的，我们接下来分部来看。
　　下面就让我们进入性能测试环节吧，这一次我们给AMD锐龙3 1300X处理器一个艰巨的任务，对比入门级的i3-6100，看看AMD锐龙3 1300X处理器性能到底能给我们带来什么样的惊喜！
测试平台：
Intel：Core i3-6100AMD：锐龙 AMD Ryzen 5 1300X
华硕Prime B250 Plus技嘉 B250M-D3H
芝奇 Trident Z RGB DDR4-3200 8G×4
SSD：三星960Pro 512GB
蓝宝石RX 580 8G D5 OC
Tt：额定 1250W DPS G RGB 1250D 电源
Windows 10 x64专业版
Fritz Chess Benchmark测试
　　Fritz Chess Benchmark是一款国际象棋测试软件，但它并不是独立存在的，而是《Fritz9》这款获得国际认可的国际象棋程序中的一个测试性能部分。Fritz Chess Benchmark是目前在个人计算机方面最好的步法计算和预测软件。
CineBench R15 跑分测试：
　　Cinebench r15中文版是一款基于Cinem4D引擎的处理器测试软件，它可以同时测试处理器子系统、内存子系统以及显示子系统。和大多数工业设计软件一样，CineBench可以完善地支持多核/多处理器，它的显示子系统测试基于OpenGL。
7-Zip测试：
　　7-Zip是一款完全免费而且开源的压缩软件，相比其他软件有更高的压缩比但同时耗费的资源也相对更多，如果你需要一款能够提供强大压缩性能的软件，那么它是你最好的选择。
　　压缩和解压过程是需要CPU不断处理大批数据，而且那些数据要求处理迅速，但也很大，所以很耗CPU和内存。我们使用7-ZIP软件里自带的性能测试工具进行跑分，来测试两款CPU的速度！
HandBrake测试
　　无需特别技巧便可直接将DVD电影内转换成AVI/MPEG4格式，还有MP4及OGM输出、AAC及Vorbis编码。HandBrake能转换被加密的（encrypted）DVD,转换时以多任务方式工作，同时让你选择语言，声音及画面质量，转换后的画面大小等。新版加入了具备x264的多线程H.264编码和H.264Baseline选项。
3Dmark测试：
　　3Dmark是Futuremark公司的一款专为测量显卡性能的软件，可以通过分数的形式向玩家展示显卡的真实性能！而现在的3Dmark已不仅仅是一款衡量显卡性能的软件，其已渐渐转变成了一款衡量整机性能的软件。
古墓丽影10(DX12 1080P)测试
　　《古墓丽影：崛起》是由Crystal Dynamics开发，Square Enix负责发行的一款单机类动作冒险游戏，该游戏是《新古墓丽影(原名：Tomb Raider，即是古墓丽影9)》的续作，于2015年12月正式发行。&
　　游戏中玩家控制女主角劳拉·克劳馥(Lara Croft)去探索她以前不相信的超自然现象和未知的世界，寻找永生的秘密。从日本龙三角的邪马台逃生后，劳拉却仍未从那次冒险的阴影里解脱出来，为了证明她在那里看到的一切并非虚无，劳拉决定跟随父亲的研究，在叙利亚寻找先知雅各的墓穴，之后前往西伯利亚，搜寻那里的神秘古城：Kitezh
守望先锋（1080P）测试：
　　《守望先锋》（Overwatch，简称OW）是由暴雪娱乐公司开发的一款第一人称射击游戏，于日全球上市，中国大陆地区由网易公司代理。游戏以未来地球为背景，讲述人类、守望先锋成员和智能机械的恩怨纠葛。游戏拥有21位英雄，每一位英雄都有各自标志性的武器和技能。
《侠盗猎车手5》测试
　　《侠盗猎车手5》（Grand Theft Auto V），是由Rockstar Games游戏公司出版发行的一款围绕犯罪为主题的开放式动作冒险游戏，游戏背景洛圣都基于现实地区中的美国洛杉矶和加州南部制作，游戏拥有几乎与现实世界相同的世界观。
《英雄联盟》测试
　　《英雄联盟》(简称LOL)是由美国拳头游戏(Riot Games)开发、中国大陆地区腾讯游戏代理运营的英雄对战MOBA竞技网游。《英雄联盟》还致力于推动全球电子竞技的发展，除了联动各赛区发展职业联赛、打造电竞体系之外，每年还会举办“季中冠军赛”“全球总决赛”“总决赛”“”“总全明星赛”三大世界级赛事，获得了亿万玩家的喜爱，形成了自己独有的电子竞技文化。
　　综上所述，通过这几轮的综合性能对比，AMD 锐龙3 1300X 处理器的游戏性能还是很优秀的，对于游戏性能的发挥上能给用户更多的惊喜！由于它不锁频，玩家还可以通过超频还可以获得额外的性能加成，进一步提升了其良好的性价比。
综合性能点评
　　Core&i3 6100与四核AMD 锐龙3 1300X 处理器的综合性能略占下风，让我们认识到了4大于2的性能差距。未来处理器的趋势一定是多核和高性价比的大方向，锐龙更加符合外来用户的使用趋势。
　　在锐龙3 1300X处理器与i3 6100都是千元之下高性价比之选，相比之下， 锐龙3 1300X 的4核心4线程是应该更会对三四线城市用户有所触动，因为未来多线程应用会是主流方向。考虑到锐龙3 1300X是具有15秒便捷超频的独有特点处理器，用户选择的天平可能会有所改变！而i3 6100方面，虽然单核性能出众，但是对比平台整体花费以及多核性能，对抗物理四核的锐龙3 1300X还是有一定的差距。AMD 锐龙3 1300X 处理器的官方价仅为899元，相信对于广大的三四线尝试玩家来说，无论网络采购，还是实体店面的购买，选择AMD 锐龙3 1300X都是比较好好的选择。
　　说到最后，AMD 锐龙3 1300X 处理器价格与i3-6100的价格相差不大，却拥有不输于i5-7500的性能！锐龙3 1300X处理器与i3 6100两款处理器都是不到千元的价格，却可以获得跨级挑战的高性能处理器产品！对于三四线玩家来说如果更看重多线程性能与超频方面的话，AMD 锐龙3 1300X非常适合你的选择，如果对于预算不敏感，而且注重单核标准的话i3 6100也可以考虑，毕竟它的性能应付日常应用也足够了，相信我们评测会给你玩家更好的选择。
用微信扫描二维码分享至好友和朋友圈
凤凰科技官方微信
播放数：1444146
播放数：497053
播放数：1867910
播放数：5808920百度搜索：
谷歌搜索：}