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Article ; Online: COVID-19 vaccines: modes of immune activation and future challenges.

Teijaro, John R / Farber, Donna L

2021 Volume 21, Issue 4, Page(s) 195–197

MeSH term(s)	2019-nCoV Vaccine mRNA-1273 ; Adaptive Immunity/immunology ; Antibodies, Neutralizing/immunology ; B-Lymphocytes/immunology ; BNT162 Vaccine ; COVID-19/prevention & control ; COVID-19 Vaccines/immunology ; COVID-19 Vaccines/therapeutic use ; ChAdOx1 nCoV-19 ; Cytokines/immunology ; Dendritic Cells/immunology ; Humans ; Immunity, Innate/immunology ; Immunologic Memory/immunology ; Interferon Type I/immunology ; Plasma Cells/immunology ; SARS-CoV-2 ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer
Chemical Substances	Antibodies, Neutralizing ; COVID-19 Vaccines ; Cytokines ; Interferon Type I ; ChAdOx1 nCoV-19 (B5S3K2V0G8) ; 2019-nCoV Vaccine mRNA-1273 (EPK39PL4R4) ; BNT162 Vaccine (N38TVC63NU)
Language	English
Publishing date	2021-03-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062776-2
ISSN	1474-1741 ; 1474-1733
ISSN (online)	1474-1741
ISSN	1474-1733
DOI	10.1038/s41577-021-00526-x
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Zs.A 5565: 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)
Zs.MG 34: Show issues

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Article ; Online: Cytokine storms in infectious diseases.

Teijaro, John R

Seminars in immunopathology

2017 Volume 39, Issue 5, Page(s) 501–503

MeSH term(s)	Animals ; Communicable Diseases/blood ; Communicable Diseases/diagnosis ; Communicable Diseases/etiology ; Communicable Diseases/therapy ; Cytokines/blood ; Humans ; Immune System/cytology ; Immune System/immunology ; Immune System/metabolism
Chemical Substances	Cytokines
Keywords	covid19
Language	English
Publishing date	2017-07-03
Publishing country	Germany
Document type	Editorial ; Introductory Journal Article
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-017-0640-2
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Zs.A 1425: Show issues

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Article ; Online: Too much of a good thing: Sustained type 1 interferon signaling limits humoral responses to secondary viral infection.

Teijaro, John R

European journal of immunology

2016 Volume 46, Issue 2, Page(s) 300–302

Abstract: The induction of a pan-immunosuppressive state is a central feature of persistent viral infections. Over the past decade, multiple pathways have been identified that contribute to immune suppression. Recently, it was revealed that aberrant or sustained ... ...

Abstract	The induction of a pan-immunosuppressive state is a central feature of persistent viral infections. Over the past decade, multiple pathways have been identified that contribute to immune suppression. Recently, it was revealed that aberrant or sustained type 1 interferon (IFN-I) production or signaling is a central contributor to immune suppression elicited during persistent viral infection. In this issue, Honke et al. [Eur. J. Immunol. 2016. 46: 372-380] identify that IFN-I signaling promotes an immune suppressive state during persistent lymphocytic choriomeningitis virus infection by inhibiting enforced virus replication in CD169(+) macrophages. The authors demonstrate that mice infected with a persistent strain of lymphocytic choriomeningitis virus have blunted humoral immune responses to a superinfecting vesicular stomatitis virus infection. The absence of virus replication in CD169(+) macrophages was not due to antiviral CD8(+) T cell-mediated killing of CD169(+) macrophages, but required sustained IFN-I responses. In turn, reduction in vesicular stomatitis virus replication in CD169(+) macrophages resulted in a reduction in antigen production, which is necessary for generating optimal humoral responses. This study highlights a novel mechanism by which IFN-I signaling promotes an immune suppressive state during persistent viral infection.
MeSH term(s)	Animals ; Antibodies, Viral/biosynthesis ; Antigen Presentation ; Antigens, Viral/immunology ; Humans ; Immunity, Humoral ; Immunosuppression ; Interferon Type I/metabolism ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/physiology ; Macrophages/immunology ; Macrophages/virology ; Mice ; Signal Transduction ; Superinfection/immunology ; Vesicular Stomatitis/immunology ; Vesiculovirus/physiology ; Virus Replication
Chemical Substances	Antibodies, Viral ; Antigens, Viral ; Interferon Type I
Language	English
Publishing date	2016-02
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201546224
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 85: Show issues

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Article ; Online: Type I interferons in viral control and immune regulation.

Teijaro, John R

Current opinion in virology

2016 Volume 16, Page(s) 31–40

Abstract: Type 1 interferons (IFN-I) exert pleiotropic biological effects during viral infections, all which contribute to balancing virus control and immune pathology. Despite extensive antiviral functions that subdue virus replication, recent studies demonstrate ...

Abstract	Type 1 interferons (IFN-I) exert pleiotropic biological effects during viral infections, all which contribute to balancing virus control and immune pathology. Despite extensive antiviral functions that subdue virus replication, recent studies demonstrate pathogenic and pro-viral roles for IFN-I signaling during acute and persistent virus infection. IFN-I signaling can promote morbidity and mortality through induction of aberrant inflammatory responses during acute viral infection. In contrast, IFN-I signaling during persistent viral infection supports immune suppression, lymphoid tissue disorganization and CD4 T cell dysfunction. Systematic characterization of the cellular populations and intricacies of IFN-I signaling that promote pathology or immune suppression during acute and persistent viral infections, respectively, should inform the development of treatments and modalities to control viral associated pathologies.
MeSH term(s)	Acute Disease ; Animals ; Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; Chronic Disease ; Humans ; Immunomodulation/drug effects ; Interferon Type I/metabolism ; Signal Transduction/drug effects ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Viral Load ; Virus Diseases/drug therapy ; Virus Diseases/etiology ; Virus Diseases/metabolism ; Virus Replication/drug effects ; Virus Replication/immunology
Chemical Substances	Antiviral Agents ; Interferon Type I
Keywords	covid19
Language	English
Publishing date	2016-01-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2611378-8
ISSN	1879-6265 ; 1879-6257
ISSN (online)	1879-6265
ISSN	1879-6257
DOI	10.1016/j.coviro.2016.01.001
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Article: The role of cytokine responses during influenza virus pathogenesis and potential therapeutic options.

Teijaro, John R

Current topics in microbiology and immunology

2015 Volume 386, Page(s) 3–22

Abstract: Aberrant pulmonary immune responses are linked to the pathogenesis of multiple human respiratory viral infections. Elevated cytokine and chemokine production "cytokine storm" has been continuously associated with poor clinical outcome and pathogenesis ... ...

Abstract	Aberrant pulmonary immune responses are linked to the pathogenesis of multiple human respiratory viral infections. Elevated cytokine and chemokine production "cytokine storm" has been continuously associated with poor clinical outcome and pathogenesis during influenza virus infection in humans and animal models. Initial trials using global immune suppression with corticosteroids or targeted neutralization of single inflammatory mediators proved ineffective to ameliorate pathology during pathogenic influenza virus infection. Thus, it was believed that cytokine storm was either chemically intractable or not causal in the pathology observed. During this review, we will discuss the history of research assessing the roles various cytokines, chemokines, and innate immune cells play in promoting pathology or protection during influenza virus infection. Several promising new strategies modulating lipid signaling have been recently uncovered for global blunting, but not ablation, of innate immune responses following influenza virus infection. Importantly, modulating lipid signaling through various means has proven effective at curbing morbidity and mortality in animal models and may be useful for curbing influenza virus induced pathology in humans. Finally, we highlight future research directions for mechanistically dissecting how modulation of lipid signaling pathways results in favorable outcomes following influenza virus infection.
MeSH term(s)	Animals ; Cytokines/physiology ; Dendritic Cells/immunology ; Humans ; Immunity, Innate ; Influenza, Human/drug therapy ; Influenza, Human/etiology ; Influenza, Human/immunology ; Macrophages/immunology ; Neutrophils/immunology
Chemical Substances	Cytokines
Language	English
Publishing date	2015
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/82_2014_411
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Article ; Online: Autoimmunity-associated allele of tyrosine phosphatase gene PTPN22 enhances anti-viral immunity.

Orozco, Robin C / Marquardt, Kristi / Pratumchai, Isaraphorn / Shaikh, Anam Fatima / Mowen, Kerri / Domissy, Alain / Teijaro, John R / Sherman, Linda A

PLoS pathogens

2024 Volume 20, Issue 3, Page(s) e1012095

Abstract: The 1858C>T allele of the tyrosine phosphatase PTPN22 is present in 5-10% of the North American population and is strongly associated with numerous autoimmune diseases. Although research has been done to define how this allele potentiates autoimmunity, ... ...

Abstract	The 1858C>T allele of the tyrosine phosphatase PTPN22 is present in 5-10% of the North American population and is strongly associated with numerous autoimmune diseases. Although research has been done to define how this allele potentiates autoimmunity, the influence PTPN22 and its pro-autoimmune allele has in anti-viral immunity remains poorly defined. Here, we use single cell RNA-sequencing and functional studies to interrogate the impact of this pro-autoimmune allele on anti-viral immunity during Lymphocytic Choriomeningitis Virus clone 13 (LCMV-cl13) infection. Mice homozygous for this allele (PEP-619WW) clear the LCMV-cl13 virus whereas wildtype (PEP-WT) mice cannot. This is associated with enhanced anti-viral CD4 T cell responses and a more immunostimulatory CD8α- cDC phenotype. Adoptive transfer studies demonstrated that PEP-619WW enhanced anti-viral CD4 T cell function through virus-specific CD4 T cell intrinsic and extrinsic mechanisms. Taken together, our data show that the pro-autoimmune allele of Ptpn22 drives a beneficial anti-viral immune response thereby preventing what is normally a chronic virus infection.
MeSH term(s)	Animals ; Mice ; Alleles ; Autoimmune Diseases/genetics ; Autoimmunity/genetics ; Lymphocytic Choriomeningitis ; Phosphoric Monoester Hydrolases/genetics ; Tyrosine
Chemical Substances	Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; Tyrosine (42HK56048U) ; Ptpn22 protein, mouse (EC 3.1.3.48)
Language	English
Publishing date	2024-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1012095
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Article ; Online: Taking down defenses to improve vaccines.

Teijaro, John R / Burton, Dennis R

Science (New York, N.Y.)

2018 Volume 359, Issue 6373, Page(s) 277–278

MeSH term(s)	Humans ; Vaccines
Chemical Substances	Vaccines
Language	English
Publishing date	2018-03-22
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aar5421
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 77: Show issues

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Article ; Online: Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.

Juarez, Ignacio / Su, Shi / Herbert, Zachary T / Teijaro, John R / Moulton, Vaishali R

Frontiers in immunology

2022 Volume 13, Page(s) 906355

Abstract: Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. ... ...

Abstract	Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.
MeSH term(s)	Animals ; Arginine ; CD8-Positive T-Lymphocytes/metabolism ; Cytokines/metabolism ; Immunity ; Mice ; RNA Splicing Factors ; Serine ; Serine-Arginine Splicing Factors/genetics ; Serine-Arginine Splicing Factors/immunology ; Serine-Arginine Splicing Factors/metabolism
Chemical Substances	Cytokines ; RNA Splicing Factors ; Srsf1 protein, mouse ; Serine-Arginine Splicing Factors (170974-22-8) ; Serine (452VLY9402) ; Arginine (94ZLA3W45F)
Language	English
Publishing date	2022-09-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.906355
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Article ; Online: B cell-derived IL-27 promotes control of persistent LCMV infection.

Pratumchai, Isaraphorn / Zak, Jaroslav / Huang, Zhe / Min, Booki / Oldstone, Michael B A / Teijaro, John R

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 3

Abstract: Recent studies have identified a critical role for B cell-produced cytokines in regulating both humoral and cellular immunity. Here, we show that B cells are an essential source of interleukin-27 (IL-27) during persistent lymphocytic choriomeningitis ... ...

Abstract	Recent studies have identified a critical role for B cell-produced cytokines in regulating both humoral and cellular immunity. Here, we show that B cells are an essential source of interleukin-27 (IL-27) during persistent lymphocytic choriomeningitis virus (LCMV) clone 13 (Cl-13) infection. By using conditional knockout mouse models with specific IL-27p28 deletion in B cells, we observed that B cell-derived IL-27 promotes survival of virus-specific CD4 T cells and supports functions of T follicular helper (Tfh) cells. Mechanistically, B cell-derived IL-27 promotes CD4 T cell function, antibody class switch, and the ability to control persistent LCMV infection. Deletion of IL-27ra in T cells demonstrated that T cell-intrinsic IL-27R signaling is essential for viral control, optimal CD4 T cell responses, and antibody class switch during persistent LCMV infection. Collectively, our findings identify a cellular mechanism whereby B cell-derived IL-27 drives antiviral immunity and antibody responses through IL-27 signaling on T cells to promote control of LCMV Cl-13 infection.
MeSH term(s)	Adaptive Immunity ; Animals ; Antibodies, Viral ; B-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/immunology ; Cytokines/metabolism ; Immunity, Cellular ; Interleukin-27/genetics ; Interleukin-27/metabolism ; Interleukins ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
Chemical Substances	Antibodies, Viral ; Cytokines ; Il27 protein, mouse ; Interleukin-27 ; Interleukins
Language	English
Publishing date	2022-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2116741119
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Zs.A 1148: Show issues

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Article ; Online: Covalent Targeting As a Common Mechanism for Inhibiting NLRP3 Inflammasome Assembly.

Stanton, Caroline / Sun, Jie / Nutsch, Kayla / Rosarda, Jessica D / Nguyen, Thu / Li-Ma, Chloris / Njomen, Evert / Melillo, Bruno / Kutseikin, Sergei / Saez, Enrique / Cravatt, Benjamin F / Teijaro, John R / Wiseman, R Luke / Bollong, Michael J

ACS chemical biology

2024 Volume 19, Issue 2, Page(s) 254–265

Abstract: The NLRP3 inflammasome is a cytosolic protein complex important for the regulation and secretion of inflammatory cytokines, including IL-1β and IL-18. Aberrant overactivation of NLRP3 is implicated in numerous inflammatory disorders. However, the ... ...

Abstract	The NLRP3 inflammasome is a cytosolic protein complex important for the regulation and secretion of inflammatory cytokines, including IL-1β and IL-18. Aberrant overactivation of NLRP3 is implicated in numerous inflammatory disorders. However, the activation and regulation of NLRP3 inflammasome signaling remain poorly understood, limiting our ability to develop pharmacologic approaches to target this important inflammatory complex. Here, we developed and implemented a high-throughput screen to identify compounds that inhibit the inflammasome assembly and activity. From this screen, we identify and profile inflammasome inhibition of 20 new covalent compounds across nine different chemical scaffolds, as well as many known inflammasome covalent inhibitors. Intriguingly, our results indicate that NLRP3 possesses numerous reactive cysteines on multiple domains whose covalent targeting blocks the activation of this inflammatory complex. Specifically, focusing on compound VLX1570, which possesses multiple electrophilic moieties, we demonstrate that this compound allows covalent, intermolecular cross-linking of NLRP3 cysteines to inhibit inflammasome assembly. Our results, along with the recent identification of numerous covalent molecules that inhibit NLRP3 inflammasome activation, further support the continued development of electrophilic compounds that target reactive cysteine residues on NLRP3 to regulate its activation and activity.
MeSH term(s)	Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Signal Transduction ; Cytokines ; Interleukin-1beta/metabolism
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Cytokines ; Interleukin-1beta
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Journal Article
ISSN	1554-8937
ISSN (online)	1554-8937
DOI	10.1021/acschembio.3c00330
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