Faculty Advisor(s): Carolyn Bertozzi, Noah Burns, Tony Wyss-Coray Jiuzhi "Gillian" Sun. Log In Sign Up. Study of the second, which ecologists call tolerance, is in its infancy. The fly is often described as having an unsophisticated and stereotypical immune response where single mutations cause simple binary changes in immunity. These results describe the first secreted feedback antagonist of Toll signalling, and demonstrate a novel Wnt activity in the fly. Most infections induce anorexia but its function, if any, remains unclear. We also found that bacteria colonized the ovary in a previously undescribed manner; bacteria were found in the posterior of the ovary, adjacent to the lateral oviduct. We recently started working on a mouse model for malaria in which we follow the progress of a Plasmodium chabaudi infection. View details for Web of Science ID 000260313000013. View details for Web of Science ID 000087913400043. Stanford Undergrad is your guide to undergraduate academics and opportunities run by the Vice Provost for Undergraduate Education. Moule, M. G., Monack, D. M., Schneider, D. S. Relating immune and stress responses to infection resistance and tolerance, The Drosophila TNF Ortholog Eiger Is Required in the Fat Body for a Robust Immune Response, The Imd Pathway Is Involved in Antiviral Immune Responses in Drosophila. We study innate immunity and microbial pathogenesis. Here we describe how the Western diet (WD), a diet high in fat and sucrose and low in fiber, found rampant in industrialized countries, leads to worse disease and poorer outcomes in an LPS-driven sepsis model in WD-fed mice compared with mice fed standard fiber-rich chow (SC). Our current focus is to determine how we recover from infections. We propose a model in which Salmonella secreted effectors stimulate the fly and thus cause an immune response that is damaging both to the bacteria and, subsequently, to the host. Victoria Chevée Laboratory Technician. Each pathogen causes a different disease as they have distinct virulence factors and niches; they each warp the health landscape in unique ways. View details for DOI 10.1371/journal.pbio, View details for Web of Science ID 000303541800003. A host has two methods to defend against pathogens: It can clear the pathogens or reduce their impact on health in other ways. Chambers, M. C., Lightfield, K. L., Schneider, D. S. Where Does Innate Immunity Stop and Adaptive Immunity Begin? Stanford Libraries' official online search tool for books, media, journals, databases, government documents and more. Taillebourgar, E., Schneider, D. S., Fauvarque, M. The ubiquitin ligase parkin mediates resistance to intracellular pathogens. Recent work in insects is helping to build our understanding of this aspect of pathology, called disease tolerance. View details for DOI 10.1371/journal.pbio.1001158. We suggest that immune responses are highly tuned by evolution, since selection for defenses that alter resistance against one pathogen may change both resistance and tolerance to other pathogens. Intracellular pathogens, which can already defeat professional phagocytes, are unaffected by eiger. We find that WD-fed mice have higher baseline inflammation (metaflammation) and signs of sepsis-associated immunoparalysis compared with SC-fed mice. View phone numbers, addresses, public records, background check reports and possible arrest records for David Schneider in San Mateo, CA. Torres, B. Y., Oliveira, J. H., Tate, A. T., Rath, P., Cumnock, K., Schneider, D. S. Drosophila melanogaster Natural Variation Affects Growth Dynamics of Infecting Listeria monocytogenes, Defining Resistance and Tolerance to Cancer, The Drosophila Deubiquitinating Enzyme dUSP36 Acts in the Hemocytes for Tolerance to Listeria monocytogenes Infections. Morbidity, the state of being diseased, is an important aspect of pathogenesis that has gone relatively unstudied in fruit flies. Because parasite rhythms matter for their fitness, understanding how they are regulated could lead to innovative ways to reduce the severity and spread of diseases. This signaling molecule is induced during infection and is required for an appropriate immune response to many microbes; however, little is known about where eiger is produced. While these studies have illuminated the effects of anorexia on infection, they consider this behavior in isolation from other behaviors and from its effects on host metabolism and energy. Health is a multidimensional landscape. Typically, studies of animal defenses focus on either understanding resistance or, to a lesser extent, tolerance mechanisms, thus providing little understanding of the relationship between these two mechanisms. Among these, we identified a class of genes including the transcription factor oxyR, and the DNA repair proteins uvrB, recB, and ruvC that help F. novicida resist oxidative stress. Dr. David Schneider grew up outside Detroit, Michigan. View details for DOI 10.1371/journal.ppat.1000111, View details for Web of Science ID 000259783000017, View details for PubMedCentralID PMC2453329. This produces characteristic phase plots that we think can be used to predict the outcome of infections and to define appropriate treatments. Moreover, our work reveals an unexpected functional link between mitophagy and infectious disease. Elrod-Erickson, M., Mishra, S., Schneider, D. A PROCESSED FORM OF THE SPATZLE PROTEIN DEFINES DORSAL-VENTRAL POLARITY IN THE DROSOPHILA EMBRYO. Here we describe the metabolic changes occurring in a model system when Listeria monocytogenes causes a lethal infection in Drosophila melanogaster. This performance has been canceled— read more. Their current focus is to determine how we recover from infections. Chambers, M. C., Song, K. H., Schneider, D. S. How the Fly Balances Its Ability to Combat Different Pathogens. Nicole Davis Graduate Student. Furthermore, overexpression of edin can induce age-dependent lethality, while loss of function in edin renders flies more susceptible to Listeria infection. These findings point to an M-CSF-producing γδ T cell subset that fulfills a specialized protective role in the later stage of malaria infection when αβ T cells have declined. To plot tolerance, individual infections are summarized by reporting the maximum parasite load and the minimum health for a population of infected individuals and the slope of the resulting curve defines the tolerance of the population. When we get sick, we want to be resilient and recover our original health. View details for DOI 10.1371/journal.pone.0041907, View details for Web of Science ID 000308788700004, View details for PubMedCentralID PMC3441536, View details for DOI 10.1073/pnas.1211724109, View details for Web of Science ID 000308565300013, View details for PubMedCentralID PMC3435157. L. monocytogenes infection also causes enzymatic reduction in the anti-oxidant uric acid, and knocking out the enzyme uric oxidase has a complicated effect on immunity. This protective effect exhibits coarse specificity for S. pneumoniae and persists for the life of the fly. Death by infection is often as much due to the host's reaction as it is to the direct result of microbial action. These results are consistent with a model in which the regulation of host factors, including edin, must be tightly controlled to avoid the detrimental consequences of having too much or too little activity. View details for DOI 10.1371/journal.pbio.0060305, View details for Web of Science ID 000261913700017, View details for PubMedCentralID PMC2596860, View details for DOI 10.1126/science.1167450, View details for Web of Science ID 000261033400028. Single-cell sequencing showed that TRAV15N-1 (Vδ6.3) γδ T cells were clonally expanded in mice and had convergent complementarity-determining region 3 sequences. In contrast, foxo mutants exhibit less wasting.In people, many infections--including tuberculosis--can cause wasting, much as we see in Drosophila. Cricket Paralysis virus (CrPV) is a member of the Dicistroviridae family of RNA viruses, which infect a broad range of insect hosts, including the fruit fly Drosophila melanogaster. Napier, B. The first, resistance, is well studied. These defense systems are thought to interact, but the nature and extent of these interactions is not known. Ann Tate A path through disease space. The survival of a bacterial pathogen within a host depends upon its ability to outmaneuver the host immune response. The top state of residence is Maryland, followed by Illinois. This suggests that attempts to extend lifespan through diet restriction or the manipulation of pathways mimicking this process will have complicated effects on a host's ability to fight infections. Such studies hold promise because they point to methods of treating infections that put evolutionary pressures on microbes different from antibiotics and vaccines. These experiments suggest that Drosophila can be used as a surrogate mosquito for defining the genetic pathways involved in both vector competence and part of the parasite sexual cycle. View details for DOI 10.1016/j.celrep.2015.09.052, View details for Web of Science ID 000363988100003. We determined that these bacterial genes are virulence factors that allow F. novicida to counteract the fly melanization immune response. Dr. Schneider's laboratory study innate immunity and microbial pathogenesis. These include both cellular immune responses, such as the phagocytosis of invading microorganisms, and humoral immune responses, such as the secretion of antimicrobial peptides into the hemolymph [1] [2]. Reciprocal Analysis of Francisella novicida Infections of a Drosophila melanogaster Model Reveal Host-Pathogen Conflicts Mediated by Reactive Oxygen and imd-Regulated Innate Immune Response. We are using a new approach to study the outcome of infections. We demonstrate that wild-typeS. Pathologic infections are accompanied by a collection of short-term behavioral perturbations collectively termed sickness behaviors [1, 2]. Here we show that parkin has a role in ubiquitin-mediated autophagy of M. tuberculosis. Less understood, however, is the effect of biotic and abiotic factors on microbial-vector interactions and the impact of the immune system on arthropod populations in nature. Parasite clearance was reduced with 2DG treatment, suggesting altered resistance. 1). We used the Plasmodium chabaudi AJ murine model of malaria as it causes severe pathology from which most animals recover. WD mice also have an increased frequency of neutrophils, some with an "aged" phenotype, in the blood during sepsis compared with SC mice. The facultative intracellular bacterial pathogen Listeria monocytogenes is capable of replicating within a broad range of host cell types and host species. This produces curves that trace the course of an infection through phase space rather than over a more typical timeline. Stanford Undergrad. These studies provide a foundation for the identification of host factors and virulence mechanisms. These maps can readily be constructed from experimental longitudinal data, and we provide two methods to generate the maps from the cross-sectional data that is commonly gathered in field trials. Three of the dominant alleles appear to cause the protein to be constitutively active and are caused by cysteine-to-tyrosine changes immediately outside the transmembrane domain. David Schneider (Professor) Manage my profile (650) 724-8064 david.schneider. All six of the remaining dominant alleles require the presence of a wild-type transmembrane Toll protein for their ventralizing effect and all encode truncated proteins that lack the transmembrane and cytoplasmic domains. The Toll protein is found around the entire dorsal-ventral circumference of the embryo, and it appears to act as a receptor for a ventral, extracellular signal and to then relay that signal to the cytoplasm in ventral regions of the embryo. Insights in the laboratory have demonstrated how the immune system provides resistance to infection, and in what manner innate defenses protect against a microbial assault. By further challenging mutant flies with L. monocytogenes mutants, we identified subgroups of fly mutants that affect specific stages of the L. monocytogenes life cycle, exit from the vacuole, or actin-based movement. View details for DOI 10.1371/journal.ppat.0030026, View details for Web of Science ID 000248495200006, View details for PubMedCentralID PMC1817657. They recently started working on a mouse model for malaria in which we follow the progress of a Plasmodium chabaudi infection. Here, we show that eiger is made in the fly's fat body during a Salmonella typhimurium infection. The functions of five Anopheles gambiae homologs were tested by using RNAi to knock down gene function followed by measuring the growth of the rodent parasite, Plasmodium berghei. Currently teaching. The screens identified genes that are involved in phagocytosis but did not detect genes known to be involved in immune signaling pathways. We conclude that the WD is reprogramming the basal immune status and acute response to LPS-driven sepsis and that this correlates with alternative disease paths that lead to more severe disease and poorer outcomes. In this issue of PLoS Biology, Konrad et al. Brenda Y. Torres A simple model of infection-induced pathology. We plot a disease tolerance curve to cancer in wild-type flies and then compare this to natural variants, identifying a line with reduced cancer resistance. Sepsis is a deleterious immune response to infection that leads to organ failure and is the 11th most common cause of death worldwide. A., Oliveira, J. H., Trujillo, D. L., Saligrama, N., Zhang, Y., Rubelt, F., Schneider, D. S., Chien, Y. H., Sauerwein, R. W., Davis, M. M. What Can Vampires Teach Us about Immunology? Professor of Medicine (Blood and Marrow Transplantation) and of Pediatrics (Stem Cell Transplantation) (650) 723-0822. In addition, we show that parasite rhythms resynchronise to the altered host feeding rhythms when food availability is shifted, which is not mediated through rhythms in the host immune system. He graduated from Wabash College in 1962 with majors in psychology and philosophy, and earned a doctorate in psychology from Stanford University in 1966. Infected hosts differ in their responses to pathogens; some hosts are resilient and recover their original health, whereas others follow a divergent path and die. Peak parasite loads were unchanged, demonstrating changes in disease tolerance. Cumnock, K., Gupta, A. S., Lissner, M., Chevee, V., Davis, N. M., Schneider, D. S. Timing of host feeding drives rhythms in parasite replication. Here, we examine the pathogenesis associated with Mycobacterium marinum infection in the fly. Free amino acid levels also change during infection, including a drop in tyrosine levels which may be due to robust L. monocytogenes induced melanization. They are using a new approach to study the outcome of infections. Torres, B. Y., Oliveira, J. H., Thomas Tate, A., Rath, P., Cumnock, K., Schneider, D. S. Tracing Personalized Health Curves during Infections, The Role of Anorexia in Resistance and Tolerance to Infections in Drosophila. The physiological response of the fly was modified further by Eiger, insulin, Wnt inhibitor of dorsal (WntD) and nitric oxide (NO) signaling. We found 6 records in 8 states for Stanford Schneider in the US. These loops enable us to track where patients lie on a typical trajectory back to health. There is no overlap between our genes and the hundreds of genes identified in Drosophila S2 cells fighting L. monocytogenes infection, using genomewide RNAi screens in vitro. We were curious whether eiger is always detrimental in the context of infection or if it plays a role in fighting some types of microbes. The sum of these two properties together defines the defensive capabilities of the host. However, activation of the Toll pathway is not sufficient for priming-induced protection. Only nine archetypical curves are needed to describe most pathogenic and mutualistic host-microbe interactions. Perhaps a way can be found using an ecological definition of tolerance, where tolerance is defined as the dose response curve of health versus parasite load. We therefore carried out a sensitized genetic screen to identify immunocompromised mutants by co-injecting beads and E. coli. Lab Alumni. As a physiatrist, he works in partnership with the orthopedic surgeons of Illinois Bone & Joint Institute to meet the diverse needs of p… This bacterium caused a lethal infection in the fly, with a 50% lethal dose (LD(50)) of 5 CFU. However, research into the pathways involved in these processes has been limited by the relatively few metrics that can be used to measure sickness and health throughout the course of infection. When looking at the matrix of signaling pathways and the microbes being tested, it was immediately obvious that most of the pathways would need to be studied in more detail before defining the rules that govern their role in pathogenesis. Drosophila has emerged as an effective system for studying innate immunity because of its powerful genetic techniques and the high degree of gene and pathway conservation. Save login - Forgot password. David Schneider Disease maps of an outbred population . By contrast, the mechanisms behind the ability to tolerate infections are studied in a less methodical manner. Sickness behaviors are important, pathogen-specific components of the host response to infection [1, 3, 7-9]. View David Schneider's business profile as Department Chair at Stanford University. Drosophila melanogaster mount an effective innate immune response against invading microorganisms, but can eventually succumb to persistent pathogenic infections. Stanford W. Ascherman, MD, FACS, Professor in Genetics (650) 723-4668. mpsnyder@stanford… Tracking Resilience to Infections by Mapping Disease Space. Gabrielle Sara Tender View details for DOI 10.1371/journal.pbio.1002435, View details for Web of Science ID 000375094800006. Upon infection, Drosophila mounts an immune response including antimicrobial peptide production and autophagy activation. Ayres, J. S., Freitag, N., Schneider, D. S. Confronting physiology: how do infected flies die? We infected the fruit fly Drosophila melanogaster with M. marinum. The purified protein is recognized by antibodies to the C-terminal half of the Spätzle protein, indicating that this polarizing activity is a product of the spätzle gene. We demonstrate that the rhythms of rodent malaria parasites in day-fed hosts become inverted relative to the rhythms of parasites in night-fed hosts. Insects are a powerful tool for discovering and then dissecting interesting new immunology. This includes reduced melanization, altered antimicrobial peptide expression and reduced feeding rates. They are making extremely mutlivariate plots of the disease process. Mutations in wntD cause susceptibility to Listeria monocytogenes infection, apparently through the derepression of Toll-Dorsal target genes, some of which are deleterious to survival. Tolerance measures the dose response curve of a host's health in reaction to a pathogen and can be studied in a simple quantitative manner. View details for DOI 10.1534/genetics.107.083782, View details for Web of Science ID 000254921600059. As we altered the system by varying host or pathogen genetics, disease tolerance varied, as we would expect if it was indeed governed by parameters controlling the sensitivity of the system (the number of bacteria required to trigger a response) and maximal effect size according to a logistic equation. Understanding how organisms fight infection has been a central focus of scientific research and medicine for the past couple of centuries, and a perennial object of trial and error by humans trying to mitigate the burden of disease. Schneider, D. S., Hudson, K. L., Lin, T. Y., Anderson, K. V. School of Earth, Energy and Environmental Sciences, Freeman Spogli Institute for International Studies, Institute for Computational and Mathematical Engineering (ICME), Institute for Human-Centered Artificial Intelligence (HAI), Institute for Stem Cell Biology and Regenerative Medicine, Stanford Institute for Economic Policy Research (SIEPR), Stanford Woods Institute for the Environment, Office of VP for University Human Resources, Office of Vice President for Business Affairs and Chief Financial Officer, Maternal & Child Health Research Institute (MCHRI), Directed Reading in Microbiology and Immunology, Microbiology and Immunology (Phd Program), DOI 10.1146/annurev-immunol-020711-075030. However, we show here that priming Drosophila with a sublethal dose of Streptococcus pneumoniae protects against an otherwise-lethal second challenge of S. pneumoniae. Both γδ T cells and M-CSF were necessary for preventing parasitemic recurrence. David schneider Associate Professor at Stanford University School of Medicine San Francisco Bay Area 79 connections We find that when plotting physiological parameters against each other, many pairs have hysteretic relationships that identify the current location of the host and predict the future route of the infection. Ellen Schneider turned up 74 matching records. Immunology textbooks teach us about the ways hosts can recognize and kill microbes but leave out something important: the mechanisms used to survive infections. We suggest that Looper will be useful in building maps of resilient immune processes across organisms. Their goal is to define "biovectors" that predict the outcome of infection and to identify the physiological mechanisms required for recovery from infections. These data indicate L. monocytogenes infection of fruit flies shares numerous features of mammalian infection, and thus that Drosophila has the potential to serve as a genetically tractable host system that will facilitate the analysis of host cellular responses to L. monocytogenes infection. We divide this review into sections mirroring these categories. Studies of infection in Drosophila melanogaster provide insight into both mechanisms of host resistance and tolerance of pathogens. View details for DOI 10.1534/g3.115.022558, View details for Web of Science ID 000367257500009. These include changes in body temperature, reduced eating and drinking, and lethargy and mimic behaviors of animals in torpor and hibernation [1, 3-6]. Our data show that antiviral innate immune responses in flies infected with CrPV depend upon hemocytes and signaling through the Imd pathway. Connect to e-resources; Report a connection problem; If we don't have it. In this study, we examined the pathogen Francisella novicida and identified new bacterial virulence factors that interact with different parts of the Drosophila melanogaster innate immune system. Schneider, D. S., JIN, Y. S., Morisato, D., Anderson, K. V. DOMINANT AND RECESSIVE MUTATIONS DEFINE FUNCTIONAL DOMAINS OF TOLL, A TRANSMEMBRANE PROTEIN REQUIRED FOR DORSAL VENTRAL POLARITY IN THE DROSOPHILA EMBRYO. Furthermore, the influence of genetic plasticity on the immune response against vector-borne pathogens remains mostly elusive. David Schneider's 14 research works with 23 citations and 334 reads, including: S3 Fig David Schneider's research while affiliated with Stanford University and other places Overview Englewood Cliffs NJ: Prentice-Hall. David Schneider Stanford School of Medicine Department of Microbiology and Immunology Fairchild Building, D300 300 Pasteur Drive Stanford, CA USA 94305-5124 Email: [email protected]. They also become hyperglycemic. Login ID: Password: Re-enter: Email: (Don't worry, your e-mail will not be distributed or made public. Bacteria were found in the cytosol of insect phagocytic cells, and were capable of directing host cell actin polymerization. Select this result to view David Schneider's phone number, address, and more. We hypothesize that resilient hosts tend to take small loops through disease space, whereas nonresilient individuals take large loops. Drosophila has highly efficient defenses against infection. A Macrophage Colony-Stimulating-Factor-Producing γδ T Cell Subset Prevents Malarial Parasitemic Recurrence. Can we clearly define "adaptive" as being different from "innate" immunity, or is it time for a more flexible description? Interactions between circadian rhythm and immunity in Drosophila melanlogaster. Scientific innovation at the intersection of disease ecology, health, and the environment. We find that growth rates and ceilings are sensitive to the initial infectious dose in a host-genotype-dependent manner, implying that experimental results differ as we change the original challenge dose within a single strain of host. This produces characteristic phase plots that they think can be used to predict the outcome of infections and to define appropriate treatments. We chose to examine the fly ovary because we found bacterial infection had a striking effect on fly reproduction. None of the identified genes have been previously implicated in innate immune responses or interactions with Plasmodium. Though either the pathogen or host immune response or both together could theoretically be the proximal cause of pathology that killed the flies, we found that the pathogen, but not the immune response, drove damage in this model. These results suggest that S. typhimurium-infected flies die from a condition that resembles TNF-induced metabolic collapse in vertebrates. (2012) in this issue of Cell Host & Microbe raises important questions about the nature of immune responses. We recovered 18 mutants with increased susceptibility to infection, none of which were previously shown to function in a Drosophila immune response. To investigate the contribution of conserved immune signaling pathways to antiviral innate immune responses, CrPV was injected into isogenic mutants of the Immune Deficiency (Imd) pathway, which resembles the mammalian Tumor Necrosis Factor Receptor (TNFR) pathway. Indeed, reports showing alternative forms of immune memory are accumulating in invertebrates. The phagocytes of Drosophila encounter bacterial invaders early in infection and contribute to survival of infection. With this new understanding of the circuitry controlling disease tolerance, we can now propose better ways of choosing, combining, and developing treatments. Brennan, C. A., Delaney, J. R., Schneider, D. S., Anderson, K. V. Bacterial infection of fly ovaries reduces egg production and induces local hernocyte activation, Akt and foxo dysregulation contribute to infection-induced wasting in Drosophila. These genes include the TNF family member eiger and the novel immunity gene edin (elevated during infection; synonym CG32185), both of which are more strongly induced by infection of wntD mutants compared to controls. Fly infections are complex and there are few simple rules that can predict how an infected fly might fare. He first came to Stanford as a postdoctoral scholar in 1996, between postdoctoral appointments at UCB and UCSF. We reasoned that the combination of anorexia and anemia would increase pressure on glycolysis as a critical energy pathway because it does not require oxygen. David Schneider. Here it is shown that the protozoan Plasmodium gallinaceum, a close relative of the human malaria parasite Plasmodium falciparum, can develop in the fruit fly Drosophila melanogaster. In the second group, mutants have a typical defense defect in which bacterial growth is increased and survival is decreased. The site facilitates research and collaboration in academic endeavors. Studies in Drosophila melanogaster have proved fruitful in determining the signals used to control NF-kappaB proteins, beginning with the discovery that the Toll/NF-kappaB pathway, in addition to patterning the dorsal-ventral axis of the fly embryo, defines a major component of the innate immune response in both Drosophila and mammals. edin is also expressed more highly during infection of wild-type flies with wild-type Salmonella typhimurium than with a less pathogenic mutant strain, and its expression is regulated in part by the Imd pathway. Department of Microbiology and Immunology Fairchild Science Building, D333 299 Campus Drive Stanford, CA 94305 Current Members. By engaging writers of this sort of fiction in an effort to solve problems in immunology we may be able to perform a directed evolution experiment where we follow the evolution of plots rather than genetic traits. Professor of Microbiology and Immunology (650) 724-8064. [email protected]. View details for DOI 10.1371/journal.pone.0050679, View details for Web of Science ID 000312386600013, View details for PubMedCentralID PMC3521769. Recent RNA interference screens that were performed at a genome-wide level have identified host factors that are important for the growth of Listeria monocytogenes in cultured cells from the fruit fly Drosophila melanogaster. Phagocytosis in flies and mammals is highly homologous: Both rely on scavenger receptors, opsonins, and actin rearrangements for engulfment; have phagosomal cysteine proteases active at low pH; and can be subverted by similar intracellular pathogens. 50 ) and of Pediatrics ( Stem Cell Transplantation ) ( 650 ) 723-4668. mpsnyder @ stanford…,. 000279152200009, View details for DOI 10.1534/genetics.108.089748, View details for Web of Science ID 000186563600005 component of the site... Health menace, killing over one million people every year and infecting about half a billion services as Professor 000301560900003... 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For infectious diseases, Stanford University United States of America of cancer biology 215 cities including new,! Enable us to track where patients lie on a typical trajectory back to health 10.1046/j.1462-5822.2003.00329.x, View details for PMC1829408! Business log in to add people & connections, or click here to create an account SC-fed mice immunity on... Well understood context of ecological interactions with their david schneider stanford toward fatty acid oxidation ketosis... Cell subset Prevents Malarial parasitemic recurrence reference question ; find a subject specialist ; using SearchWorks ; Connection foxo.

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