可以. 服务费为总费用15%

 In recent years there have been major advances in our understanding of the mechanisms that are involved in the recognition of microbes and subsequent activation of host immune defenses. Several classes of membrane-bound and cytosolic pattern recognition receptors (PRRs) have been identified and partially characterized. These include the Toll-like receptors (TLRs), NOD-like receptors (NLRs) and RIG-I-like receptors (RLRs). Activation of PRRs leads to the production of a large array of pro-inflammatory and anti-microbial molecules that are critical for the elimination of invading pathogens and activation of adaptive immune responses. A class of cytosolic PRRs is involved in the assembly of the inflammasome, a molecular platform that mediates activation of caspase-1 and secretion of mature IL-1b and IL-18. Importantly, activation of the inflammasome is also induced by non-microbial mechanisms including endogenous molecules involved in the pathogenesis of metabolic and inflammatory diseases. In addition, there is evidence that autophagy, a cellular process that mediates recycling of intracellular components, is involved in microbial recognition and plays a key role in host defense. The initial sensing of microbes often occurs at mucosal surfaces, but the interplay between recognition of commensal vs. pathogenic microbes on the host immune system is only beginning to be uncovered. The goal of the Keystone Symposia meeting on Innate Immunity: Sensing the Microbes and Damage Signals is to gather scientists working on innate immunity to discuss cutting-edge research on the mechanisms that regulate the activation of the immune system by microbes as well as by endogenous damage signals, and to integrate such knowledge in the context of inflammation, homeostasis, host defense and disease. Opportunities for interdisciplinary interactions will be significantly enhanced by the concurrent meeting on The Microbiome, which will share a keynote address and three plenary sessions with this meeting.

近年来已有重大进展，在我们的理解，在微生物的识别和随后激活宿主的免疫防御机制。已经确定的几个类的膜结合型和胞浆内模式识别受体（PRRS）和部分特点。这些措施包括Toll样受体（TLRs），NOD样受体（NLRs）和RIG - I样受体（RLRs）。 PRRS激活导致一个大阵亲抗炎和抗微生物的分子，是为消灭入侵的病原体和适应性免疫反应的激活的关键生产。 A类胞质PRRS参与炎性大会，分子平台，激活介导的caspase - 1和成熟的IL - 1B和IL - 18的分泌。更重要的是，激活炎性也是诱发非微生物机制，包括参与代谢和炎症性疾病的发病机制的内源性分子。此外，有证据表明，吞噬，介导细胞内成分的回收一个细胞的过程，是涉及微生物识别和发挥了关键作用，在宿主防御。微生物的初步传感常发生在粘膜表面，但承认共生宿主的免疫系统与病原微生物之间的相互作用才刚刚开始被发现。梯形专题讨论会会议上的先天免疫的目标：检测的微生物和损害信号收集先天免疫工作的科学家讨论尖端的研究机制，规范由微生物以及免疫系统的激活内源性损害信号，并整合在炎症，动态平衡，宿主防御和疾病等知识。跨学科的互动的机会将显着增强的同时，将与本次会议上发表专题演说和三次全体会议上的微生物群系会议。

 每年一届　

 1.以上标注"可以"的服务项目可单独办理.
 2.单项服务的费用以最终确认单为准.
 3.参会整体流程服务费1000人民币/人.
   服务费包含:代送签证、代订往返机票、代订当地酒店.  
   服务费不含:各项目所产生的实际费用.

 如您有其他需求或建议请点击这里.

 汇率计算以付款时中国工商银行外汇卖出价为准.

 咨询电话: 8610-66054455  8610-51294800   设诉电话: 8610-66054488
 在线客服: MSN:fanmeiguojikefu@hotmail.com    QQ:1391456367