U.S. Veterinary Immune Reagent Network
U.S. Veterinary Immune Reagent Network
NEW for March 2013:
All pages have been updated with monoclonal information and recent publications and presentations. Please check individual pages for information related to that species.
Click here for a listing of all publications and presentations related to U.S. VIRN since 2005.
Species pages contain targeted molecule updates and indices of commercially available reagents. The buttons below provide Network-wide information.
To request reagents produced by the US VIRN initiative, please contact the people listed below:
(cytokines, chemokines, cell surface markers)
Antibodies
Recombinant Cytokines & Chemokines
Not currently available
Chicken & Turkey
Not currently available
The buttons below provide information about available reagents from US VIRN project directors (Kingfisher Biotech, Inc) and sister European initiatives (The Immunological Toolbox).
Project Description:
A major obstacle to disease control in cattle,
chickens, pigs, horses and fish is the lack of sufficient immunological
reagents. The goal of the US-VIRN is to generate monoclonal antibodies (mAb)
that identify the major leukocyte subpopulations (T and B lymphocytes, NK
cells, macrophages, dendritic cells, neutrophils), antibody classes and produce
bioactive recombinant cytokines and chemokines as well as antibodies to them
and their receptors for these species. These reagents will be used to: (1)
evaluate changes during disease and following vaccination and (2) give
scientests the ability to manipulate immune system cells to ascertain their
roles in protective immunity as well as in immunopathology. Development of the
above reagents will address the USDA-CSREES goal of enhancing the safety of the
Nation's agriculture and food supply by aiding in the development of vaccines.
Products developed
will benefit a large group of researchers,
including veterinary clinicians, immunologists, pathologists, and
microbiologists.
Project Funding
USDA NIFA #-20649
Peter Johnson, DVM, Ph.D. , Co-Director
Margo Holland, DVM, Ph.D. , Co-Director
Click here for the US-VIRN PDs Workshop presentation presented at CRWAD, December 2012.
Last updated: March 2013
For further information about the U.S. Veterinary Immune Reagent Network, contact
University of Massachusetts Amherst.
For information about the US VIRN website, contact , University of Massachusetts Amherst.
Project Directors:
Catfish: Dr. Melanie Wilson & Dr. Eva Bengten,University of Mississippi Medical Center
Equine: Dr. Bettina Wagner, Cornell University
Poultry: Dr. Hyun Lillehoj,
USDA-ARS (Maryland
Cattle: Dr. Cynthia Baldwin,
University of Massachusetts
Pig: Dr. Joan Lunney,
USDA-ARS (Maryland)
Trout: Dr. John Hansen, Western Fisheries Research Center, USG &
Dr. Erin Bromage, University of Massachusetts Dartmouth
Protein Expression: Kingfisher Biotech &
Dr. Bettina Wagner,
Cornell University
Advisory Board:
Dr. Douglas Antczak
Cornell University
Dr. Gary Entrican
International Union Immunological Society Veterinary Toolkit Committee
Dr. Cyril Gay
USDA-ARS, National Program Leader
Dr. John Liu
Alabama Agricultural Experiment Station
Dr. Michael Murtaugh
University of Minnesota
Dr. Rebecca Poston
Pfizer Animal Health
Dr. Shayan Sharif
University of OntarioGuelph, Canada
Dr. Jagdev Sharma
Arizona State University Biodesign Institute
Dr. Greg Wiens
USDA-ARS, Kearneysville, WV
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食物过敏原的低过敏性处理方法及其评价体系研究进展.pdf 7页
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第 31卷 第4期
分析测试学报
Vo1．3lNo．4
FENXICESHIXUEBAO(JournalofInstrumentalAnalysis)
；综 述 ；
h !， !／! ! 墨
食物过敏原的低过敏性处理方法
及其评价体系研究进展
孙佳益，王锡 昌，刘 源，卢 瑛
(上海海洋大学 食品学院 上海水产品加工及贮藏工程技术研究中心，上海 201306)
摘 要：食物过敏是由食物引起的机体对免疫系统的异常反应 ，近几十年来 ，世界范围内食物过敏反应症患
者呈逐年上升趋势，食物过敏已成为一个新兴的食品安全 题。极其微量的过敏原即能导致一些患者出现强
烈的过敏反应，因此寻求降低食物过敏原的活性处理方法显得格外重要。该文综述了近年来关于食物过敏原
的低过敏性处理方法及其评价体系的研究进展，通过对低过敏性生物处理方法中的酶解法 、物理方法和生物
物理结合法 ，以及食物过敏原性的体外评价方法和动物模型评价体系进行对比分析和讨论 ，探讨了食物过敏
原的低过敏性处理方法及其评价体系的发展方向。
关键词：食物；过敏原；低过敏性；处理方法；体外评价 ；动物模型；研究进展
中图分类号 ：R392．3；G353．11
文献标识码 ：A
文章编号：(95—07
doi：l0．3969／j．issn．．3
ResearchAdvancesonHypoallergenicProcessingMethodsofFood
AllergensandtheirEvaluationSystems
SUNJia—yi，WANG Xi-chang，LIUYuan，LU Ying
(CollegeofFoodScienceandTechnology，ShanghaiOceanUniversity，ShanghaiEngineeringResearchCenter
ofAquaticProductProcessing，Shanghai 201306，China)
Abstract：Foodallergyisanabnormalresponseoforganism totheimmunesystem causedbyfoods．
Inrecentdecades，Foodallergypatientshasrisengraduallyworldwideandfoodallergyhasbecome
anemergingissueoffoodsafety． Itisimportanttofindprocessingmethodstoreducefoodanaphylaxis
asextremelytraceoftheallergenCaBmakesomepatientsexperiencestrongallergicreaction． Inthis
paper，hypoallergenicprocessingmethodsoffoodallergenandtheircorrespondingevaluationsystems
inrecentyearsarereviewed． Enzymatichydrolysismethod，physicalmethodsandbiochemicalcoin—
biningphysicalmethodsareanalysed，andthemethodsofinvitroevaluationandanimalmodelevalu—
ationsystem offoodallergenicityarecompared．Thedevelopmentdirectionofhypoallergenieprocess—
ingmethodsoffoodallergenandtheirevaluation systemsar
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he immune system is the body’s defender. It identifies, tracks
down, and destroys troublemakers before they can hurt the body. Those
troublemakers may be, for example, bacteria from a cut or splinter, a measles
germ, a cold bug, or even a cancer cell.
These invaders try to take over our tissues and feed off our
bodies’ nutrients. If they succeed, we become sick or, sometimes, even die.
It’s the job of our immune systems to destroy these invaders before they
destroy us.
Say you picked up a flu virus(病毒) last week. Perhaps it entered your body through a cut, from a
drinking glass, or from the air you breathe. Of course, you didn’t feel it, but
the virus made its way into your bloodstream. As soon as it entered your body,
it began to reproduce. Viruses have only one goal: to take over your cells.
Once inside your body, viruses try to enter cells and disrupt their normal
work. If left alone, these viruses would hurt so many cells that you would
weaken, or worse, get a serious illness.
But this flu virus should not be so complacent as it seems to be.
As it reproduces in your bloodstream, the virus is met by a certain kind of
white blood cell, the lymphocytes. The lymphocytes are the foot soldiers that
keep you alive.
The number of lymphocytes in your body is hard to imagine.
Thousands of them could fit in the period at the end of this sentence. Your
body holds about a trillion —that’s 1,000,000,000,000 of them, or about 3,000 in every drop of blood. Since you began reading this sentence, over 800,000 of them have been created and destroyed.
Some of these lymphocytes pass through a small walnut-sized organ
called the thymus(胸腺). The thymus is
the base of the neck. Here, special hormones(荷尔蒙)turn lymphocytes into fighting cells, called T cells.
T cells have one terrific talent: They can tell the difference
be what should be in our bodies and what shouldn’t. They
do not affect the body ’s healthy cells. Yet they attack everything that is
foreign to our bodies, such as germs, transplants, and even our own cells which
have become abnormal, as in the case of cancer.
71.What is
the function of our immune system?
A. To take
over our tissues and feed off our bodies’ nutrients.
prevent bacteria or germs from entering the body.
destroy the troublemakers in order that they might not hurt the body.
D. To fight
against T cells.
72.What does
the word “lymphocytes” mean?
soldiers.&&&& &B. Flu virus.&&&& C.
White blood cells. &&&D. Troublemakers.
73.The last
sentence in paragraph 5 “since you began reading this sentence, over 800,000 of
them have been created and destroyed” implies that ____.
sentence contributes to the increase of the number of lymphocytes in your body
B. you would
not realize that lymphocytes reproduce themselves rapidly but for this sentence
C. because
you read this sentence, a large number of lymphocytes have been consumed
number of lymphocytes in your body is extremely large
74.Which of
the following can NOT be detected(察觉) by T cells?
Thymus.&& B. Transplants.&& C. Cancer
cells.&&& D. Healthy cells.
如果没有找到你要的答案，请尝试下下面的试题答案搜索功能。
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备课中心教案课件试卷下载E-cigarette vapor boosts superbugs and dampens immune system | EurekAlert! Science News
E-cigarette vapor boosts superbugs and dampens immune system
In lab and mouse experiments, exposure promotes bacterial virulence and inflammation, while blocking the body's ability to fight infection
University of California - San Diego
Researchers at the University of California, San Diego School of Medicine and Veterans Affairs San Diego Healthcare System report data suggesting that e-cigarettes are toxic to human airway cells, suppress immune defenses and alter inflammation, while at the same time boosting bacterial virulence. The mouse study is published January 25 by the Journal of Molecular Medicine.
"This study shows that e-cigarette vapor is not benign -- at high doses it can directly kill lung cells, which is frightening," said senior author Laura E. Crotty Alexander, MD, staff physician at the Veterans Affairs San Diego Healthcare System and assistant clinical professor at UC San Diego School of Medicine. "We already knew that inhaling heated chemicals, including the e-liquid ingredients nicotine and propylene glycol, couldn't possibly be good for you. This work confirms that inhalation of e-cigarette vapor daily leads to changes in the inflammatory milieu inside the airways."
Crotty Alexander reported the preliminary results of this work at the American Thoracic Society annual meetings in 2014 and 2015. But now her team has also seen their findings hold up in mice. Inflammatory markers -- signs of full-body inflammation -- in the airways and blood of mice that inhaled e-cigarette vapors for one hour a day, five days a week, for four weeks were elevated by 10 percent compared to unexposed mice.
"We don't know specifically which lung and systemic diseases will be caused by the inflammatory changes induced by e-cigarette vapor inhalation, but based on clinical reports of acute toxicities and what we have found in the lab, we believe that they will cause disease in the end," Crotty Alexander said. "Some of the changes we have found in mice are also found in the airways and blood of conventional cigarette smokers, while others are found in humans with cancer or inflammatory lung diseases."
Conversely, bacterial pathogens exposed to e-cigarette vapor benefited. Specifically, Staphylococcus aureus bacteria were better able to form biofilms, adhere to and invade airway cells and resist human antimicrobial peptides after exposure to e-cigarette vapor.
E-cigarette vapor extract-exposed bacteria were also more virulent in a mouse model of pneumonia. All mice infected with normal methicillin-resistant S. aureus (MRSA), an antibiotic-resistant "superbug," survived. Meanwhile, 25 percent of mice infected with MRSA pre-exposed to e-cigarette vapor died.
The results were consistent with e-liquids from seven different manufacturers, demonstrating that the findings are not limited to one formula or brand.
Crotty Alexander and team also
that MRSA bacteria exposed to conventional cigarette smoke are more resistant to killing by the immune system than unexposed bacteria.
Study co-authors include John H. Hwang, Veterans Affairs San Diego Healthcare System and UC San D Matthew Lyes, VA San Diego Healthcare System and Duke U Katherine Sladewski, Denzil P. Mathew, Alexander Moshensky, VA San Diego Healthcare S Shymaa Enany, Suez Canal University and VA San Diego Healthcare S Elisa K. McEachern, VA San Diego Healthcare System and Weill Cornell Medical C Soumita Das, David T. Pride, Weg M. Ongkeko, UC San D and Sagar Bapat, Salk Institute for Biological Studies.
This research was funded by the U.S. Department of Veterans Affairs.
Related Journal ArticleDifferential immune-related gene expression in the spleens of duck Tembusu virus-infected goslings - ScienceDirect
ExportJavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page., December 2017, Pages 39-47Author links open overlay panelShow moreAbstractFlaviviruses pose a significant threat to public health worldwide. Recently, a novel flavivirus, duck Tembusu virus (TMUV), was identified as the causative agent of a serious duck viral disease in Asia. Its rapid spread and expanded host range have raised substantial concerns regarding its potential threat to non-avian hosts, including humans. However, the specific molecular host responses to this virus are poorly understood. In this study, we used the RNA-sequencing technique to analyse the differential gene expression in the spleens of infected goslings 5 days post-infection. In total, 2878 upregulated unigenes and 2943 downregulated unigenes were identified. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that different pattern recognition receptor (PRR) signalling pathways simultaneously participated in the sensing of the pathogen-associated molecular patterns (PAMPs) of TMUV, and the antigen presentation pathway and acquired immunity were activated. Then, the signals were transduced by the NF-kappa B (NF-κB) or the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathways, resulting in the enormous production of various cytokines and interferon-stimulated genes (ISGs). We further investigated the immune response patterns in the liver and brain tissue using RT-qPCR. The bacterial peptidoglycan sensor nucleotide-binding oligomerization domain-containing protein 1 (NOD1) receptor was significantly upregulated, especially in the brain tissue, suggesting that NOD1 likely induces an inflammatory response by interacting with dsRNA, which is similar to its actions during hepatitis C viral (HCV) infection. However, major histocompatibility complex II (MHCII) was downregulated only in the spleen, indicating that the downregulation of MHCII in the spleen may be an immune evasion strategy of TMUV to facilitate pathogenesis during infection. Here, we are the first to report a transcriptome analysis of the host immune response to TMUV infection, and the data reported herein may help elucidate the molecular mechanisms of the gosling-TMUV interaction.KeywordsTMUVGoslingTranscriptome analysisImmune responseChoose an option to locate/access this article:Check if you have access through your login credentials or your institution.ororRecommended articlesCiting articles (0)