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Spatiotemporal Fluctuation Induced Transition in a Tumor Model with Immune Surveillance  [PDF]
Wei-Rong Zhong,Yuan-Zhi Shao,Zhen-Hui He
Physics , 2006, DOI: 10.1103/PhysRevE.74.011916
Abstract: We report on a simple model of spatial extend anti-tumor system with a fluctuation in growth rate, which can undergo a nonequilibrium phase transition. Three states as excited, sub-excited and non-excited states of a tumor are defined to describe its growth. The multiplicative noise is found to be double-face: The positive effect on a non-excited tumor and the negative effect on an excited tumor.
The role of the microenvironment in tumor immune surveillance  [cached]
Oluwadayo Oluwadara,Luca Giacomelli,Xenia Brant,Russell Christensen4
Bioinformation , 2011,
Abstract: The evidence appears compelling that the microenvironment, and associated biological cellular and molecular factors, may contribute to the progression of a variety of tumors. The effects of the microenvironment may directly influence the plasticity of T cell lineages, which was recently discussed (O’Shea & Paul, 2010 ). To review the putative role of the microenvironment in modulating the commitment of tumor immune surveillance, we use the model of oral premalignant lesions.
Tumor-Associated Glycans and Immune Surveillance  [PDF]
Behjatolah Monzavi-Karbassi,Anastas Pashov,Thomas Kieber-Emmons
Vaccines , 2013, DOI: 10.3390/vaccines1020174
Abstract: Changes in cell surface glycosylation are a hallmark of the transition from normal to inflamed and neoplastic tissue. Tumor-associated carbohydrate antigens (TACAs) challenge our understanding of immune tolerance, while functioning as immune targets that bridge innate immune surveillance and adaptive antitumor immunity in clinical applications. T-cells, being a part of the adaptive immune response, are the most popular component of the immune system considered for targeting tumor cells. However, for TACAs, T-cells take a back seat to antibodies and natural killer cells as first-line innate defense mechanisms. Here, we briefly highlight the rationale associated with the relative importance of the immune surveillance machinery that might be applicable for developing therapeutics.
The Synthesis of Truncated Polypeptides for Immune Surveillance and Viral Evasion  [PDF]
Sylvain Cardinaud,Shelley R. Starck,Piyanka Chandra,Nilabh Shastri
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008692
Abstract: Cytotoxic T cells detect intracellular pathogens by surveying peptide loaded MHC class I molecules (pMHC I) on the cell surface. Effective immune surveillance also requires infected cells to present pMHC I promptly before viral progeny can escape. Rapid pMHC I presentation apparently occurs because infected cells can synthesize and present peptides from antigenic precursors called defective ribosomal products (DRiPs). The molecular characteristics of DRiPs are not known.
Immune surveillance of nasopharyngeal carcinoma (NpC)
Oluwadayo O Oluwadara,Andre Barkhordarian,Luca Giacomelli,Xenia Brant
Bioinformation , 2011,
Abstract: In the U.S., nasopharyngeal carcinoma (NpC) kills >7,600 each year. Deaths are predominantly among adult men, and in most cases, early detection and treatment can save lives. Despite the annual spending of approximately 3.2 billion dollars on head and neck cancer research, NpC remains a neglected disease since its fatality rates are among the lowest nation wide. The relative survival rates from NpC have not improved in the U.S. in the last 20 years. Infection with Epstein Barr Virus (EBV) is an important co-factor in the etiology of NpC. In other regions of the word (e.g., South-East Asia, Latin America), EBV infection and NpC-related prevalence and mortality are substantially higher and more alarming. Epidemiological data indicate high prevalence of EBV infection and increased risk for NpC among Central and South American and Asian immigrants in the U.S., and also predict a sharp increase in NpC incidence in the next decade. To face this emerging threat, it is important to develop and validate novel modes of detection and intervention for NpC. To this end, we characterized the proteomic signature of NpC, and of the tumor infiltrating lymphocytes of the CD8+, activated (CD38+, mTOR+) and regulatory immune cell (FoxP3+) phenotype. Paraffinized biopsies were processed, and tissue microarrays constructed and tested by immunohistochemistry and tri-immunohistofluorescence for a battery of signaling markers, including AKT and PI3K, in conjunction with EBV status and ANKRD11, an NpC susceptibility biomarker. Microphotographs, analyzed and quantified by confocal microscopy and fractal analysis, suggest new avenues for immunotherapies of NpC.
Initiation and Regulation of CNS Autoimmunity: Balancing Immune Surveillance and Inflammation in the CNS  [PDF]
Melissa G. Harris, Zsuzsanna Fabry
Neuroscience & Medicine (NM) , 2012, DOI: 10.4236/nm.2012.33026
Abstract: While the central nervous system (CNS) was once thought to be immune privileged, more recent data support that certain areas of the healthy CNS are routinely patrolled by immune cells. Further, antigen drainage is another means by which the adaptive arm of the immune system can gain information about the health of the CNS. Altogether these ensure that the CNS is not beyond the scope of immune protection against viruses and tumors. However, immune surveillance in the CNS has to be tightly regulated, as CNS autoimmune disease and inflammation may arise from increased immune cell infiltration. In this review we discuss the concept and implications of CNS immune surveillance and introduce the CNS antigen-presenting cells (APCs) that potentially regulate neuroinflammation and autoimmunity. We also discuss novel animal models in which CNS disease initiation and the role of APCs in disease regulation can be tested.
Unraveling a Three-Step Spatiotemporal Mechanism of Triggering of Receptor-Induced Nipah Virus Fusion and Cell Entry  [PDF]
Qian Liu,Jacquelyn A. Stone,Birgit Bradel-Tretheway,Jeffrey Dabundo,Javier A. Benavides Montano,Jennifer Santos-Montanez,Scott B. Biering,Anthony V. Nicola,Ronald M. Iorio,Xiaonan Lu,Hector C. Aguilar
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003770
Abstract: Membrane fusion is essential for entry of the biomedically-important paramyxoviruses into their host cells (viral-cell fusion), and for syncytia formation (cell-cell fusion), often induced by paramyxoviral infections [e.g. those of the deadly Nipah virus (NiV)]. For most paramyxoviruses, membrane fusion requires two viral glycoproteins. Upon receptor binding, the attachment glycoprotein (HN/H/G) triggers the fusion glycoprotein (F) to undergo conformational changes that merge viral and/or cell membranes. However, a significant knowledge gap remains on how HN/H/G couples cell receptor binding to F-triggering. Via interdisciplinary approaches we report the first comprehensive mechanism of NiV membrane fusion triggering, involving three spatiotemporally sequential cell receptor-induced conformational steps in NiV-G: two in the head and one in the stalk. Interestingly, a headless NiV-G mutant was able to trigger NiV-F, and the two head conformational steps were required for the exposure of the stalk domain. Moreover, the headless NiV-G prematurely triggered NiV-F on virions, indicating that the NiV-G head prevents premature triggering of NiV-F on virions by concealing a F-triggering stalk domain until the correct time and place: receptor-binding. Based on these and recent paramyxovirus findings, we present a comprehensive and fundamentally conserved mechanistic model of paramyxovirus membrane fusion triggering and cell entry.
A Distinct Translation Initiation Mechanism Generates Cryptic Peptides for Immune Surveillance  [PDF]
Shelley R. Starck, Yongkai Ow, Vivian Jiang, Maria Tokuyama, Mark Rivera, Xin Qi, Richard W. Roberts, Nilabh Shastri
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003460
Abstract: MHC class I molecules present a comprehensive mixture of peptides on the cell surface for immune surveillance. The peptides represent the intracellular protein milieu produced by translation of endogenous mRNAs. Unexpectedly, the peptides are encoded not only in conventional AUG initiated translational reading frames but also in alternative cryptic reading frames. Here, we analyzed how ribosomes recognize and use cryptic initiation codons in the mRNA. We find that translation initiation complexes assemble at non-AUG codons but differ from canonical AUG initiation in response to specific inhibitors acting within the peptidyl transferase and decoding centers of the ribosome. Thus, cryptic translation at non-AUG start codons can utilize a distinct initiation mechanism which could be differentially regulated to provide peptides for immune surveillance.
Infiltrative microgliosis: activation and long-distance migration of subependymal microglia following periventricular insults
W Shawn Carbonell, Shin-Ichi Murase, Alan F Horwitz, James W Mandell
Journal of Neuroinflammation , 2005, DOI: 10.1186/1742-2094-2-5
Abstract: We have developed and characterized a novel model for the investigation of subventricular microglial reactions in mice using intracerebroventricular (ICV) injection of high-dose rhodamine dyes. Dynamic studies using timelapse confocal microscopy in situ complemented the histopathological analysis.We demonstrate that high-dose ICV rhodamine dye injection resulted in selective uptake by the ependyma and ependymal death within hours. Phagocytosis of ependymal debris by activated SVMs was evident by 1d as demonstrated by the appearance of rhodamine-positive SVMs. In the absence of further manipulation, labelled SVMs remained in the subventricular space. However, these cells exhibited the ability to migrate several hundred microns into the parenchyma towards a deafferentation injury of the hippocampus. This "infiltrative microgliosis" was verified in situ using timelapse confocal microscopy. Finally, supporting the disease relevance of this event, the triad of ependymal cell death, SVM activation, and infiltrative microgliosis was recapitulated by a single ICV injection of HIV-1 tat protein.Subependymal microglia exhibit robust activation and migration in periventricular inflammatory responses. Further study of this population of microglia may provide insight into neurological diseases with tendencies to involve the ventricular system and periventricular tissues.It has become increasingly evident that the central nervous system is an immunocompetent organ [1]. Microglia are the primary immune effector cells of the brain parenchyma and functionally resemble tissue macrophages elsewhere in the body [1,2]. The brain ventricles are also under immune surveillance by intraventricular macrophages which patrol the cerebrospinal fluid (CSF), choroid plexus, and supraependymal surface [3]. At the interface of the CSF and brain proper is the ciliated neuroepithelial ependymal cell which lines the ventricular system of the brain and spinal canal. The ependyma not only functions as a
Surveillance of febrile patients in a district and evaluation of their spatiotemporal associations: a pilot study
Kin-wing Choi, Ngai-sze Wong, Lap-yip Lee, Shui-shan Lee
BMC Public Health , 2010, DOI: 10.1186/1471-2458-10-84
Abstract: We captured consecutive emergency department visits that led to hospitalization in a district hospital in Hong Kong during the period of 12 Sep 2005 to 14 Oct 2005. We recorded demographic data, provisional diagnoses, temperature on presentation and residential location for each patient-episode, and geocoded the residential addresses. We applied Geographical Information System technology to study the geographical distribution these cases, and their associations within a 50-m buffer zone spatially. A case cluster was defined by three or more spatially associated febrile patients within each three consecutive days.One thousand and sixty six patient-episodes were eligible for analysis; 42% of them had fever (>37°C; oral temperature) on presentation. Two hundred and four patient-episodes (19.1%) came from residential care homes for elderly (RCHE). We detected a total of 40 case clusters during the study period. Clustered cases were of older age; 57 (33.3%) were residents of RCHE. We found a median of 3 patients (range: 3 - 8) and time span of 3 days (range: 2 - 8 days) in each cluster. Twenty five clusters had 2 or more patients living in the same building block; 18 of them were from RCHE.It is technically feasible to perform surveillance on febrile patients and studying their spatiotemporal associations. The information is potentially useful for early detection of impending infectious disease threats.With the lessons learnt from the severe acute respiratory syndrome (SARS) epidemic in 2003 and heightened awareness on emerging infectious diseases, e.g. avian influenza [1,2], there has been a clear demand globally on effective infectious disease surveillance mechanisms that can achieve early event detection and health situational awareness. As a result, automated syndromic surveillance systems have emerged in recent years, and its applicability has been evaluated in various studies. Most of these reported studies focused on emergency department visits, and data were grou
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