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Article ; Online: ExRNA Takes a Toll in Sepsis-associated Lung Injury.

Lam, L K Metthew / Mangalmurti, Nilam S

American journal of respiratory cell and molecular biology

2022 Volume 67, Issue 3, Page(s) 271–272

MeSH term(s)	Humans ; Lung Injury ; MicroRNAs ; Respiratory Distress Syndrome ; Sepsis/complications ; Toll-Like Receptor 7/genetics
Chemical Substances	MicroRNAs ; TLR7 protein, human ; Toll-Like Receptor 7
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2022-0237ED
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Article ; Online: Inflammatory and tissue injury marker dynamics in pediatric acute respiratory distress syndrome.

Yehya, Nadir / Booth, Thomas J / Ardhanari, Gnana D / Thompson, Jill M / Lam, L K Metthew / Till, Jacob E / Mai, Mark V / Keim, Garrett / McKeone, Daniel J / Halstead, E Scott / Lahni, Patrick / Varisco, Brian M / Zhou, Wanding / Carpenter, Erica L / Christie, Jason D / Mangalmurti, Nilam S

The Journal of clinical investigation

2024

Abstract: Background: The molecular signature of pediatric acute respiratory distress syndrome (ARDS) is poorly described, and the degree to which hyperinflammation or specific tissue injury contributes to outcomes is unknown. Therefore, we profiled inflammation ... ...

Abstract	Background: The molecular signature of pediatric acute respiratory distress syndrome (ARDS) is poorly described, and the degree to which hyperinflammation or specific tissue injury contributes to outcomes is unknown. Therefore, we profiled inflammation and tissue injury dynamics over the first 7 days of ARDS, and associated specific biomarkers with mortality, persistent ARDS, and persistent multiple organ dysfunction syndrome (MODS). Methods: In a single-center prospective cohort of intubated pediatric ARDS, we collected plasma on days 0, 3, and 7. Nineteen biomarkers reflecting inflammation, tissue injury, and damage associated molecular patterns were measured. We assessed the relationship between biomarkers and trajectories with mortality, persistent ARDS, or persistent MODS using multivariable mixed effect models. Results: In 279 subjects (64 [23%] non-survivors), hyperinflammatory cytokines, tissue injury markers, and DAMPs were higher in non-survivors. Survivors and non-survivors showed different biomarker trajectories. IL-1α, sTNFR1, ANG2, and SPD increased in non-survivors, while DAMPs remained persistently elevated. ANG2 and P3NP were associated with persistent ARDS, whereas multiple cytokines, tissue injury markers, and DAMPs were associated with persistent MODS. Corticosteroid use did not impact the association of biomarker levels or trajectory with mortality. Conclusions: Pediatric ARDS survivors and non-survivors had distinct biomarker trajectories, with cytokines, endothelial and alveolar epithelial injury, and DAMPs elevated in non-survivors. Mortality markers overlapped with markers associated with persistent MODS, rather than persistent ARDS.
Language	English
Publishing date	2024-04-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI177896
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Article ; Online: Bat Red Blood Cells Express Nucleic Acid-Sensing Receptors and Bind RNA and DNA.

Lam, L K Metthew / Dobkin, Jane / Eckart, Kaitlyn A / Gereg, Ian / DiSalvo, Andrew / Nolder, Amber / Anis, Eman / Ellis, Julie C / Turner, Greg / Mangalmurti, Nilam S

ImmunoHorizons

2022 Volume 6, Issue 5, Page(s) 299–306

Abstract: RBCs demonstrate immunomodulatory capabilities through the expression of nucleic acid sensors. However, little is known about bat RBCs, and no studies have examined the immune function of bat erythrocytes. In this study, we show that bat RBCs express the ...

Abstract	RBCs demonstrate immunomodulatory capabilities through the expression of nucleic acid sensors. However, little is known about bat RBCs, and no studies have examined the immune function of bat erythrocytes. In this study, we show that bat RBCs express the nucleic acid-sensing TLRs TLR7 and TLR9 and bind the nucleic acid ligands, ssRNA, and CpG DNA. Collectively, these data suggest that, like human RBCs, bat erythrocytes possess immune function and may be reservoirs for nucleic acids. These findings provide unique insight into bat immunity and may uncover potential mechanisms by which virulent pathogens of humans are concealed in bats.
MeSH term(s)	Animals ; Chiroptera/genetics ; DNA ; Erythrocytes ; Humans ; Nucleic Acids ; RNA
Chemical Substances	Nucleic Acids ; RNA (63231-63-0) ; DNA (9007-49-2)
Language	English
Publishing date	2022-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2573-7732
ISSN (online)	2573-7732
DOI	10.4049/immunohorizons.2200013
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Article ; Online: Gamma-interferon exerts a critical early restriction on replication and dissemination of yellow fever virus vaccine strain 17D-204.

Lam, L K Metthew / Watson, Alan M / Ryman, Kate D / Klimstra, William B

NPJ vaccines

2018 Volume 3, Page(s) 5

Abstract: Live attenuated viruses are historically among the most effective viral vaccines. Development of a safe vaccine requires the virus to be less virulent, a phenotype that is historically arrived by empirical evaluation often leaving the mechanisms of ... ...

Abstract	Live attenuated viruses are historically among the most effective viral vaccines. Development of a safe vaccine requires the virus to be less virulent, a phenotype that is historically arrived by empirical evaluation often leaving the mechanisms of attenuation unknown. The yellow fever virus 17D live attenuated vaccine strain has been developed as a delivery vector for heterologous antigens; however, the mechanisms of attenuation remain elusive. The successful and safe progress of 17D as a vaccine vector and the development of live attenuated vaccines (LAVs) to related flaviviruses requires an understanding of the molecular mechanisms leading to attenuation. Using subcutaneous infection of interferon-deficient mouse models of wild type yellow fever virus (WT YFV) pathogenesis and 17D-mediated immunity, we found that, in the absence of type I IFN (IFN-α/β), type II interferon (IFN-γ) restricted 17D replication, but not that of WT YFV, by 1-2 days post-infection. In this context, IFN-γ responses protected 17D-infected animals from mortality, largely restricted the virus to lymphoid organs, and eliminated viscerotropic disease signs such as steatosis in the liver and inflammatory cell infiltration into the spleen. However, WT YFV caused a disseminated infection, gross liver pathology, and rapid death of the animals. In vitro, IFN-γ treatment of myeloid cells suppressed the replication of 17D significantly more than that of WT YFV, suggesting a direct differential effect on 17D virus replication. Together these data indicate that an important mechanism of 17D attenuation in vivo is increased sensitivity to IFN-γ stimulated responses elicited early after infection.
Language	English
Publishing date	2018-01-23
Publishing country	England
Document type	Journal Article
ISSN	2059-0105
ISSN (online)	2059-0105
DOI	10.1038/s41541-017-0039-z
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Article ; Online: Biochemical characterization of ethanol-dependent reduction of furfural by alcohol dehydrogenases.

Li, Qunrui / Metthew Lam, L K / Xun, Luying

Biodegradation

2011 Volume 22, Issue 6, Page(s) 1227–1237

Abstract: ... had high affinities for NADH (e.g., K ( d ... of 0.043 μM for the FurX-NADH complex) and relatively low affinities for NAD(+) (e.g., K ...

Abstract	Lignocellulosic biomass is usually converted to hydrolysates, which consist of sugars and sugar derivatives, such as furfural. Before yeast ferments sugars to ethanol, it reduces toxic furfural to non-inhibitory furfuryl alcohol in a prolonged lag phase. Bioreduction of furfural may shorten the lag phase. Cupriavidus necator JMP134 rapidly reduces furfural with a Zn-dependent alcohol dehydrogenase (FurX) at the expense of ethanol (Li et al. 2011). The mechanism of the ethanol-dependent reduction of furfural by FurX and three homologous alcohol dehydrogenases was investigated. The reduction consisted of two individual reactions: ethanol-dependent reduction of NAD(+) to NADH and then NADH-dependent reduction of furfural to furfuryl alcohol. The kinetic parameters of the coupled reaction and the individual reactions were determined for the four enzymes. The data indicated that limited NADH was released in the coupled reaction. The enzymes had high affinities for NADH (e.g., K ( d ) of 0.043 μM for the FurX-NADH complex) and relatively low affinities for NAD(+) (e.g., K ( d ) of 87 μM for FurX-NAD(+)). The kinetic data suggest that the four enzymes are efficient "furfural reductases" with either ethanol or NADH as the reducing power. The standard free energy change (ΔG°') for ethanol-dependent reduction of furfural was determined to be -1.1 kJ mol(-1). The physiological benefit for ethanol-dependent reduction of furfural is likely to replace toxic and recalcitrant furfural with less toxic and more biodegradable acetaldehyde.
MeSH term(s)	Alcohol Dehydrogenase/chemistry ; Alcohol Dehydrogenase/genetics ; Alcohol Dehydrogenase/isolation & purification ; Alcohol Dehydrogenase/metabolism ; Amino Acid Sequence ; Bacterial Proteins/chemistry ; Bacterial Proteins/genetics ; Bacterial Proteins/isolation & purification ; Bacterial Proteins/metabolism ; Cloning, Molecular ; Cupriavidus necator/enzymology ; Cupriavidus necator/genetics ; Escherichia coli/enzymology ; Escherichia coli/genetics ; Ethanol/metabolism ; Furaldehyde/metabolism ; Furans/metabolism ; Industrial Microbiology ; Isoenzymes/chemistry ; Isoenzymes/genetics ; Isoenzymes/isolation & purification ; Isoenzymes/metabolism ; Kinetics ; Molecular Sequence Data ; NAD/metabolism ; Phylogeny ; Plasmids ; Pseudomonas aeruginosa/enzymology ; Pseudomonas aeruginosa/genetics ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/enzymology ; Sequence Alignment ; Thermodynamics ; Transformation, Bacterial
Chemical Substances	Bacterial Proteins ; Furans ; Isoenzymes ; Recombinant Proteins ; NAD (0U46U6E8UK) ; Ethanol (3K9958V90M) ; furfuryl alcohol (D582054MUH) ; Furaldehyde (DJ1HGI319P) ; Alcohol Dehydrogenase (EC 1.1.1.1)
Language	English
Publishing date	2011-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1056014-2
ISSN	1572-9729 ; 0923-9820
ISSN (online)	1572-9729
ISSN	0923-9820
DOI	10.1007/s10532-011-9477-x
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Article ; Online: Cupriavidus necator JMP134 rapidly reduces furfural with a Zn-dependent alcohol dehydrogenase.

Li, Qunrui / Metthew Lam, L K / Xun, Luying

Biodegradation

2011 Volume 22, Issue 6, Page(s) 1215–1225

Abstract: Ethanol is a renewable biofuel, and it can be produced from lignocellulosic biomass. The biomass is usually converted to hydrolysates that consist of sugar and sugar derivatives, such as furfural. Yeast ferments sugar to ethanol, but furfural higher than ...

Abstract	Ethanol is a renewable biofuel, and it can be produced from lignocellulosic biomass. The biomass is usually converted to hydrolysates that consist of sugar and sugar derivatives, such as furfural. Yeast ferments sugar to ethanol, but furfural higher than 3 mM is inhibitory. It can take several days for yeast cells to reduce furfural to non-inhibitory furfuryl alcohol before producing ethanol. Bioreduction of furfural to furfuryl alcohol before fermentation may relieve yeast from furfural toxicity. We observed that Cupriavidus necator JMP134, a strict aerobe, rapidly reduced 17 mM furfural to less than 3 mM within 14 min with cell turbidity of 1.0 at 600 nm at 50°C. The rapid reduction consumed ethanol. The "furfural reductase" (FurX) was purified, and it oxidized ethanol to acetaldehyde and reduced furfural to furfuryl alcohol with NAD(+) as the cofactor. The protein was identified with mass spectrometry fingerprinting to be a hypothetical protein belonging to Zn-dependent alcohol dehydrogenase family. The furX-inactivation mutant of C. necator JMP134 lost the ability to rapidly reduce furfural, and Escherichia coli producing recombinant FurX gained the ability. Thus, an alcohol dehydrogenase enabled bacteria to rapidly reduce furfural with ethanol as the reducing power.
MeSH term(s)	Alcohol Dehydrogenase/chemistry ; Alcohol Dehydrogenase/genetics ; Alcohol Dehydrogenase/isolation & purification ; Alcohol Dehydrogenase/metabolism ; Bacterial Proteins/chemistry ; Bacterial Proteins/genetics ; Bacterial Proteins/isolation & purification ; Bacterial Proteins/metabolism ; Biomass ; Cloning, Molecular ; Cupriavidus necator/enzymology ; Cupriavidus necator/genetics ; Escherichia coli/enzymology ; Escherichia coli/genetics ; Ethanol/metabolism ; Fermentation ; Furaldehyde/metabolism ; Furans/metabolism ; Industrial Microbiology ; Kinetics ; Lignin/metabolism ; NAD/metabolism ; Oxidation-Reduction ; Plasmids ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/metabolism ; Transformation, Bacterial ; Zinc/metabolism
Chemical Substances	Bacterial Proteins ; Furans ; Recombinant Proteins ; NAD (0U46U6E8UK) ; lignocellulose (11132-73-3) ; Ethanol (3K9958V90M) ; Lignin (9005-53-2) ; furfuryl alcohol (D582054MUH) ; Furaldehyde (DJ1HGI319P) ; Alcohol Dehydrogenase (EC 1.1.1.1) ; Zinc (J41CSQ7QDS)
Language	English
Publishing date	2011-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1056014-2
ISSN	1572-9729 ; 0923-9820
ISSN (online)	1572-9729
ISSN	0923-9820
DOI	10.1007/s10532-011-9476-y
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Article ; Online: Host translation shutoff mediated by non-structural protein 2 is a critical factor in the antiviral state resistance of Venezuelan equine encephalitis virus.

Bhalla, Nishank / Sun, Chengqun / Metthew Lam, L K / Gardner, Christina L / Ryman, Kate D / Klimstra, William B

Virology

2016 Volume 496, Page(s) 147–165

Abstract: Most previous studies of interferon-alpha/beta (IFN-α/β) response antagonism by alphaviruses have focused upon interruption of IFN-α/β induction and/or receptor signaling cascades. Infection of mice with Venezuelan equine encephalitis alphavirus (VEEV) ... ...

Abstract	Most previous studies of interferon-alpha/beta (IFN-α/β) response antagonism by alphaviruses have focused upon interruption of IFN-α/β induction and/or receptor signaling cascades. Infection of mice with Venezuelan equine encephalitis alphavirus (VEEV) or Sindbis virus (SINV) induces serum IFN-α/β, that elicits a systemic antiviral state in uninfected cells successfully controlling SINV but not VEEV replication. Furthermore, VEEV replication is more resistant than that of SINV to a pre-existing antiviral state in vitro. While host macromolecular shutoff is proposed as a major antagonist of IFN-α/β induction, the underlying mechanisms of alphavirus resistance to a pre-existing antiviral state are not fully defined, nor is the mechanism for the greater resistance of VEEV. Here, we have separated viral transcription and translation shutoff with multiple alphaviruses, identified the viral proteins that induce each activity, and demonstrated that VEEV nonstructural protein 2-induced translation shutoff is likely a critical factor in enhanced antiviral state resistance of this alphavirus.
MeSH term(s)	Animals ; Antiviral Agents/metabolism ; Antiviral Agents/pharmacology ; Cell Line ; Disease Resistance ; Encephalitis Virus, Venezuelan Equine/drug effects ; Encephalitis Virus, Venezuelan Equine/physiology ; Encephalomyelitis, Venezuelan Equine/genetics ; Encephalomyelitis, Venezuelan Equine/metabolism ; Encephalomyelitis, Venezuelan Equine/mortality ; Encephalomyelitis, Venezuelan Equine/virology ; Horses ; Host-Pathogen Interactions ; Humans ; Interferons/biosynthesis ; Interferons/pharmacology ; Mice ; Mutation ; Phenotype ; Protein Biosynthesis ; RNA, Viral ; Viral Nonstructural Proteins/genetics ; Viral Nonstructural Proteins/metabolism
Chemical Substances	Antiviral Agents ; RNA, Viral ; Viral Nonstructural Proteins ; Interferons (9008-11-1)
Language	English
Publishing date	2016-06-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2016.06.005
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Article ; Online: DNA binding to TLR9 expressed by red blood cells promotes innate immune activation and anemia.

Lam, L K Metthew / Murphy, Sophia / Kokkinaki, Dimitra / Venosa, Alessandro / Sherrill-Mix, Scott / Casu, Carla / Rivella, Stefano / Weiner, Aaron / Park, Jeongho / Shin, Sunny / Vaughan, Andrew E / Hahn, Beatrice H / Odom John, Audrey R / Meyer, Nuala J / Hunter, Christopher A / Worthen, G Scott / Mangalmurti, Nilam S

Science translational medicine

2021 Volume 13, Issue 616, Page(s) eabj1008

Abstract: Red blood cells (RBCs) are essential for aerobic respiration through delivery of oxygen to distant tissues. However, RBCs are currently considered immunologically inert, and few, if any, secondary functions of RBCs have been identified. Here, we showed ... ...

Abstract	Red blood cells (RBCs) are essential for aerobic respiration through delivery of oxygen to distant tissues. However, RBCs are currently considered immunologically inert, and few, if any, secondary functions of RBCs have been identified. Here, we showed that RBCs serve as critical immune sensors through surface expression of the nucleic acid–sensing Toll-like receptor 9 (TLR9). Mammalian RBCs expressed TLR9 on their surface and bound CpG-containing DNA derived from bacteria, plasmodia, and mitochondria. RBC-bound mitochondrial DNA was increased during human and murine sepsis and pneumonia. In vivo, CpG-carrying RBCs drove accelerated erythrophagocytosis and innate immune activation characterized by increased interferon signaling. Erythroid-specific deletion of TLR9 abrogated erythrophagocytosis and decreased local and systemic cytokine production during CpG-induced inflammation and polymicrobial sepsis. Thus, detection and capture of nucleic acid by TLR9-expressing RBCs regulated red cell clearance and inflammatory cytokine production, demonstrating that RBCs function as immune sentinels during pathologic states. Consistent with these findings, RBC-bound mitochondrial DNA was elevated in individuals with viral pneumonia and sepsis secondary to coronavirus disease 2019 (COVID-19) and associated with anemia and severity of disease. These findings uncover a previously unappreciated role of RBCs as critical players in inflammation distinct from their function in gas transport.
MeSH term(s)	Anemia ; Animals ; DNA ; Erythrocytes ; Humans ; Immunity, Innate ; Mice ; Toll-Like Receptor 9
Chemical Substances	TLR9 protein, human ; Toll-Like Receptor 9 ; DNA (9007-49-2)
Language	English
Publishing date	2021-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abj1008
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Article ; Online: Erythrocytes identify complement activation in patients with COVID-19.

Lam, L K Metthew / Reilly, John P / Rux, Ann H / Murphy, Sophia J / Kuri-Cervantes, Leticia / Weisman, Ariel R / Ittner, Caroline A G / Pampena, M Betina / Betts, Michael R / Wherry, E John / Song, Wen-Chao / Lambris, John D / Meyer, Nuala J / Cines, Douglas B / Mangalmurti, Nilam S

American journal of physiology. Lung cellular and molecular physiology

2021 Volume 321, Issue 2, Page(s) L485–L489

Abstract: COVID-19, the disease caused by the SARS-CoV-2 virus, can progress to multisystem organ failure and viral sepsis characterized by respiratory failure, arrhythmias, thromboembolic complications, and shock with high mortality. Autopsy and preclinical ... ...

Abstract	COVID-19, the disease caused by the SARS-CoV-2 virus, can progress to multisystem organ failure and viral sepsis characterized by respiratory failure, arrhythmias, thromboembolic complications, and shock with high mortality. Autopsy and preclinical evidence implicate aberrant complement activation in endothelial injury and organ failure. Erythrocytes express complement receptors and are capable of binding immune complexes; therefore, we investigated complement activation in patients with COVID-19 using erythrocytes as a tool to diagnose complement activation. We discovered enhanced C3b and C4d deposition on erythrocytes in COVID-19 sepsis patients and non-COVID sepsis patients compared with healthy controls, supporting the role of complement in sepsis-associated organ injury. Our data suggest that erythrocytes may contribute to a precision medicine approach to sepsis and have diagnostic value in monitoring complement dysregulation in COVID-19-sepsis and non-COVID sepsis and identifying patients who may benefit from complement targeted therapies.
MeSH term(s)	COVID-19/complications ; COVID-19/immunology ; COVID-19/virology ; Complement Activation/immunology ; Complement C3b/immunology ; Complement C3b/metabolism ; Complement C4b/immunology ; Complement C4b/metabolism ; Erythrocytes/immunology ; Erythrocytes/metabolism ; Erythrocytes/virology ; Female ; Humans ; Male ; Middle Aged ; Peptide Fragments/immunology ; Peptide Fragments/metabolism ; Respiratory Insufficiency/diagnosis ; Respiratory Insufficiency/immunology ; Respiratory Insufficiency/metabolism ; Respiratory Insufficiency/virology ; SARS-CoV-2/isolation & purification ; Sepsis/diagnosis ; Sepsis/immunology ; Sepsis/metabolism ; Sepsis/virology
Chemical Substances	Peptide Fragments ; Complement C3b (80295-43-8) ; Complement C4b (80295-50-7) ; complement C4d (80295-52-9)
Language	English
Publishing date	2021-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00231.2021
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Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: The 17D-204 Vaccine Strain-Induced Protection against Virulent Yellow Fever Virus Is Mediated by Humoral Immunity and CD4+ but not CD8+ T Cells.

Alan M Watson / L K Metthew Lam / William B Klimstra / Kate D Ryman

PLoS Pathogens, Vol 12, Iss 7, p e

2016 Volume 1005786

Abstract: A gold standard of antiviral vaccination has been the safe and effective live-attenuated 17D-based yellow fever virus (YFV) vaccines. Among more than 500 million vaccinees, only a handful of cases have been reported in which vaccinees developed a ... ...

Abstract	A gold standard of antiviral vaccination has been the safe and effective live-attenuated 17D-based yellow fever virus (YFV) vaccines. Among more than 500 million vaccinees, only a handful of cases have been reported in which vaccinees developed a virulent wild type YFV infection. This efficacy is presumed to be the result of both neutralizing antibodies and a robust T cell response. However, the particular immune components required for protection against YFV have never been evaluated. An understanding of the immune mechanisms that underlie 17D-based vaccine efficacy is critical to the development of next-generation vaccines against flaviviruses and other pathogens. Here we have addressed this question for the first time using a murine model of disease. Similar to humans, vaccination elicited long-term protection against challenge, characterized by high neutralizing antibody titers and a robust T cell response that formed long-lived memory. Both CD4+ and CD8+ T cells were polyfunctional and cytolytic. Adoptive transfer of immune sera or CD4+ T cells provided partial protection against YFV, but complete protection was achieved by transfer of both immune sera and CD4+ T cells. Thus, robust CD4+ T cell activity may be a critical contributor to protective immunity elicited by highly effective live attenuated vaccines.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2016-07-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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