可编程数据平面(Programmable Data Plane,PDP)允许用户自定义网络设备的数据包处理方式,支持定制化网络操作,利用PDP的特性实施网络防御,在实时性、灵活性、扩展性等方面取得了良好效果,近年来受到学术界和工业界的广泛关注。本文以基...可编程数据平面(Programmable Data Plane,PDP)允许用户自定义网络设备的数据包处理方式,支持定制化网络操作,利用PDP的特性实施网络防御,在实时性、灵活性、扩展性等方面取得了良好效果,近年来受到学术界和工业界的广泛关注。本文以基于PDP的网络防御技术为主要研究内容,首先介绍了PDP的基本概念,并结合典型案例阐述其应用于网络防御的优势;随后根据实施网络防御的阶段,将基于PDP的网络防御技术分为防护技术、检测技术、响应技术3大类,对各类方案的现有研究进行深入分析、概括总结,归纳不同方法的优缺点;最后,本文对基于PDP的网络防御技术未来的研究方向进行展望。展开更多
针对语音通信系统中由于干扰、音频源不稳定等因素导致的接收端语音突变或响度不一致的问题,提出一种变步长最小均方误差自适应增益控制(VSSLMS-AGC,variable step size least mean square-adaptive gain control)新方案。该方案首先利...针对语音通信系统中由于干扰、音频源不稳定等因素导致的接收端语音突变或响度不一致的问题,提出一种变步长最小均方误差自适应增益控制(VSSLMS-AGC,variable step size least mean square-adaptive gain control)新方案。该方案首先利用指数加权移动平均记录历史梯度信息,以此来调节最小均方误差算法的步长,使算法收敛速度更快,稳态误差更小;然后将变步长思想运用到自动增益控制中,确保能够自适应地调节语音增益值,使原先幅值不一的音频信号输出范围恒定且不失原有的特性,降低语音落差,改善听觉感受。展开更多
Regulatory T cells(Treg cells)are a specialized subset of CD4+T cells defined by expression of the lineage-specifying transcription factor FOXP3 and a potent capacity to maintain peripheral immune tolerance.The modern...Regulatory T cells(Treg cells)are a specialized subset of CD4+T cells defined by expression of the lineage-specifying transcription factor FOXP3 and a potent capacity to maintain peripheral immune tolerance.The modern concept of Tregs was catalyzed by Shimon Sakaguchi's identification of CD4+CD25+suppressive T cells and subsequent work establishing FOXP3 as a central determinant of Treg cell development and function;together with landmark FOXP3 genetic discoveries by Mary E.Brunkow and Fred Ramsdell,these advances transformed understanding of immune homeostasis and were recognized by the 2025 Nobel Prize in Physiology or Medicine.Under normal physiological conditions,FOXP3+Treg cells restrain autoreactive lymphocytes,prevent excessive inflammation,and shape antigen-presenting cell activity through contact-dependent pathways and suppressive cytokines,thereby protecting tissues from immune-mediated damage.Disruption of Treg abundance,stability,or suppressive capacity can therefore lead to immune dysregulation and disease.Over the past two decades,Treg cells have become a major focus of immunology because their roles are highly context-dependent.In autoimmune and chronic inflammatory diseases,impaired Treg cell function or insufficient Treg activity contributes to loss of tolerance and persistent tissue injury,supporting therapeutic approaches designed to enhance Treg cell number,stability,and suppressive potency.In contrast,many cancers exploit Treg cells by promoting their expansion,activation,and recruitment into the tumor microenvironment(TME),where they blunt antitumor immunity by suppressing cytotoxic T-cell priming and effector function,limiting dendritic cell activation,and fostering immune escape.In both settings,immune checkpoint pathways critically influence Treg cell biology.Beyond PD-1/PD-L1 and CTLA-4,emerging checkpoints and costimulatory receptors,including TIGIT,TIM-3,LAG-3,and OX40,modulate Treg cell generation,stability,and suppressive functions,thereby shaping the balance between tolerance and immunity.Meanwhile,immunometabolic adaptations further tune Treg cell fitness and function in inflamed tissues and tumors;lipid utilization and mitochondrial programs,among other metabolic axes,enable Treg cells to persist in nutrient-and oxygen-restricted microenvironments,while microenvironmental stress can drive functional remodeling or fragility in a subset-dependent manner.In this review,we summarize the discovery and defining biological features of Treg cells,highlight core suppressive mechanisms and regulatory circuits,and synthesize evidence for the dual roles of Treg cells in preventing autoimmunity yet enabling tumor immune evasion.We further outline current and emerging therapeutic strategies aimed at augmenting Treg cell activity to restore tolerance in autoimmune disease,or selectively depleting,functionally inhibiting,and reprogramming tumor-resident Treg cells to enhance cancer immunotherapy.Overall we discuss how deeper insight into Treg heterogeneity,checkpoint control,and immunometabolic regulation may enable more precise Treg celldirected interventions and inform next-generation immunotherapeutic combinations across immune-mediated and malignant diseases.展开更多
文摘可编程数据平面(Programmable Data Plane,PDP)允许用户自定义网络设备的数据包处理方式,支持定制化网络操作,利用PDP的特性实施网络防御,在实时性、灵活性、扩展性等方面取得了良好效果,近年来受到学术界和工业界的广泛关注。本文以基于PDP的网络防御技术为主要研究内容,首先介绍了PDP的基本概念,并结合典型案例阐述其应用于网络防御的优势;随后根据实施网络防御的阶段,将基于PDP的网络防御技术分为防护技术、检测技术、响应技术3大类,对各类方案的现有研究进行深入分析、概括总结,归纳不同方法的优缺点;最后,本文对基于PDP的网络防御技术未来的研究方向进行展望。
文摘针对语音通信系统中由于干扰、音频源不稳定等因素导致的接收端语音突变或响度不一致的问题,提出一种变步长最小均方误差自适应增益控制(VSSLMS-AGC,variable step size least mean square-adaptive gain control)新方案。该方案首先利用指数加权移动平均记录历史梯度信息,以此来调节最小均方误差算法的步长,使算法收敛速度更快,稳态误差更小;然后将变步长思想运用到自动增益控制中,确保能够自适应地调节语音增益值,使原先幅值不一的音频信号输出范围恒定且不失原有的特性,降低语音落差,改善听觉感受。
文摘Regulatory T cells(Treg cells)are a specialized subset of CD4+T cells defined by expression of the lineage-specifying transcription factor FOXP3 and a potent capacity to maintain peripheral immune tolerance.The modern concept of Tregs was catalyzed by Shimon Sakaguchi's identification of CD4+CD25+suppressive T cells and subsequent work establishing FOXP3 as a central determinant of Treg cell development and function;together with landmark FOXP3 genetic discoveries by Mary E.Brunkow and Fred Ramsdell,these advances transformed understanding of immune homeostasis and were recognized by the 2025 Nobel Prize in Physiology or Medicine.Under normal physiological conditions,FOXP3+Treg cells restrain autoreactive lymphocytes,prevent excessive inflammation,and shape antigen-presenting cell activity through contact-dependent pathways and suppressive cytokines,thereby protecting tissues from immune-mediated damage.Disruption of Treg abundance,stability,or suppressive capacity can therefore lead to immune dysregulation and disease.Over the past two decades,Treg cells have become a major focus of immunology because their roles are highly context-dependent.In autoimmune and chronic inflammatory diseases,impaired Treg cell function or insufficient Treg activity contributes to loss of tolerance and persistent tissue injury,supporting therapeutic approaches designed to enhance Treg cell number,stability,and suppressive potency.In contrast,many cancers exploit Treg cells by promoting their expansion,activation,and recruitment into the tumor microenvironment(TME),where they blunt antitumor immunity by suppressing cytotoxic T-cell priming and effector function,limiting dendritic cell activation,and fostering immune escape.In both settings,immune checkpoint pathways critically influence Treg cell biology.Beyond PD-1/PD-L1 and CTLA-4,emerging checkpoints and costimulatory receptors,including TIGIT,TIM-3,LAG-3,and OX40,modulate Treg cell generation,stability,and suppressive functions,thereby shaping the balance between tolerance and immunity.Meanwhile,immunometabolic adaptations further tune Treg cell fitness and function in inflamed tissues and tumors;lipid utilization and mitochondrial programs,among other metabolic axes,enable Treg cells to persist in nutrient-and oxygen-restricted microenvironments,while microenvironmental stress can drive functional remodeling or fragility in a subset-dependent manner.In this review,we summarize the discovery and defining biological features of Treg cells,highlight core suppressive mechanisms and regulatory circuits,and synthesize evidence for the dual roles of Treg cells in preventing autoimmunity yet enabling tumor immune evasion.We further outline current and emerging therapeutic strategies aimed at augmenting Treg cell activity to restore tolerance in autoimmune disease,or selectively depleting,functionally inhibiting,and reprogramming tumor-resident Treg cells to enhance cancer immunotherapy.Overall we discuss how deeper insight into Treg heterogeneity,checkpoint control,and immunometabolic regulation may enable more precise Treg celldirected interventions and inform next-generation immunotherapeutic combinations across immune-mediated and malignant diseases.
