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Article ; Online: You are the tumor queen, microbiome fiend, IL-17.

Jana, Jessica A / Overacre-Delgoffe, Abigail E

2024 Volume 57, Issue 1, Page(s) 11–13

Abstract: The role of IL-17 signaling in cancer remains convoluted due to its role in regulating the gut microbiome. In a recent issue of Cancer Cell, Chandra et al. demonstrate that microbially driven IL-17 signaling promotes tumor growth. ...

Abstract	The role of IL-17 signaling in cancer remains convoluted due to its role in regulating the gut microbiome. In a recent issue of Cancer Cell, Chandra et al. demonstrate that microbially driven IL-17 signaling promotes tumor growth.
MeSH term(s)	Humans ; Interleukin-17 ; Microbiota ; Gastrointestinal Microbiome ; Neoplasms ; Signal Transduction
Chemical Substances	Interleukin-17
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2023.12.011
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Zs.A 4227: 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: Regulation of tissue-resident memory T cells by the Microbiota.

Overacre-Delgoffe, Abigail E / Hand, Timothy W

Mucosal immunology

2022 Volume 15, Issue 3, Page(s) 408–417

Abstract: Resident memory T cells (Trms) predominantly reside within tissue and are critical for providing rapid protection against invasive viruses, fungi and bacteria. Given that tissues are heavily impacted and shaped by the microbiota, it stands to reason that ...

Abstract	Resident memory T cells (Trms) predominantly reside within tissue and are critical for providing rapid protection against invasive viruses, fungi and bacteria. Given that tissues are heavily impacted and shaped by the microbiota, it stands to reason that Trms are also influenced by the microbiota that inhabits barrier sites. The influence of the microbiota is largely mediated by microbial production of metabolites which are crucial to the immune response to both viral infection and cancerous tumors. In addition to the effects of metabolites, antigens derived from the microbiota can activate T cell responses. While microbiota-specific T cells may assist in tissue repair, control of infection and anti-tumor immunity, the actual 'memory' potential of these cells remains unclear. Here, we hypothesize that memory responses to antigens from the microbiota must be 'licensed' by inflammatory signals activated by invasion of the host by microorganisms.
MeSH term(s)	Bacteria ; Humans ; Immunity ; Memory T Cells ; Microbiota ; Neoplasms
Language	English
Publishing date	2022-02-22
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-022-00491-1
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Article ; Online: Promoter IV-BDNF deficiency disturbs cholinergic gene expression of CHRNA5, CHRM2, and CHRM5: effects of drug and environmental treatments.

Sakata, Kazuko / Overacre, Abigail E

Journal of neurochemistry

2017 Volume 143, Issue 1, Page(s) 49–64

Abstract: Brain-derived neurotrophic factor (BDNF) promotes maturation of cholinergic neurons. However, how activity-dependent BDNF expression affects specific cholinergic gene expression remains unclear. This study addressed this question by determining mRNA ... ...

Abstract	Brain-derived neurotrophic factor (BDNF) promotes maturation of cholinergic neurons. However, how activity-dependent BDNF expression affects specific cholinergic gene expression remains unclear. This study addressed this question by determining mRNA levels of 22 acetylcholine receptor subunits, the choline transporter (CHT), and the choline acetyltransferase (ChAT) in mice deficient in activity-dependent BDNF via promoter IV (KIV) and control wild-type mice. Quantitative RT-PCR revealed significant reductions in nicotinic acetylcholine receptor alpha 5 (CHRNA5) in the frontal cortex and hippocampus and M5 muscarinic acetylcholine receptor (CHRM5) in the hippocampus, but significant increases in M2 muscarinic acetylcholine receptor (CHRM2) in the frontal cortex of KIV mice compared to wild-type mice. Three-week treatments with fluoxetine, phenelzine, duloxetine, imipramine, or an enriched environment treatment (EET) did not affect the altered expression of these genes except that EET increased CHRNA5 levels only in KIV frontal cortex. EET also increased levels of CHRNA7, CHT, and ChAT, again only in the KIV frontal cortex. The imipramine treatment was most prominent among the four antidepressants; it up-regulated hippocampal CHRM2 and frontal cortex CHRM5 in both genotypes, and frontal cortex CHRNA7 only in KIV mice. To the best of our knowledge, this is the first evidence that BDNF deficiency disturbs expression of CHRNA5, CHRM2, and CHRM5. Our results suggest that promoter IV-BDNF deficiency - which occurs under chronic stress - causes cholinergic dysfunctions via these receptors. EET is effective on CHRNA5, while its compensatory induction of other cholinergic genes or drugs targeting CHRNA5, CHRM2, and CHRM5 may become an alternative strategy to reverse these BDNF-linked cholinergic dysfunctions.
MeSH term(s)	Animals ; Antidepressive Agents/pharmacology ; Brain-Derived Neurotrophic Factor/deficiency ; Brain-Derived Neurotrophic Factor/genetics ; Environment ; Female ; Frontal Lobe/drug effects ; Frontal Lobe/metabolism ; Gene Expression ; Hippocampus/drug effects ; Hippocampus/metabolism ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/physiology ; Receptor, Muscarinic M2/biosynthesis ; Receptor, Muscarinic M2/genetics ; Receptor, Muscarinic M5/biosynthesis ; Receptor, Muscarinic M5/genetics ; Receptors, Nicotinic/biosynthesis ; Receptors, Nicotinic/genetics
Chemical Substances	Antidepressive Agents ; Brain-Derived Neurotrophic Factor ; CHRM2 protein, human ; CHRNA5 protein, mouse ; Receptor, Muscarinic M2 ; Receptor, Muscarinic M5 ; Receptors, Nicotinic
Language	English
Publishing date	2017-08-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.14129
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Article ; Online: T(reg) stability: to be or not to be.

Overacre, Abigail E / Vignali, Dario Aa

Current opinion in immunology

2016 Volume 39, Page(s) 39–43

Abstract: Regulatory T cell (T(reg)) stability has been primarily determined by the maintained expression of the transcription factor Forkhead box P3 (Foxp3). However, T(regs) can exhibit instability while maintaining Foxp3 expression, requiring a re-examination ... ...

Abstract	Regulatory T cell (T(reg)) stability has been primarily determined by the maintained expression of the transcription factor Forkhead box P3 (Foxp3). However, T(regs) can exhibit instability while maintaining Foxp3 expression, requiring a re-examination of what defines T(reg) stability. Recent work suggests that the establishment and stability of T(regs) is mediated by a number of mechanisms besides Foxp3 expression, such as epigenetic modifications, Foxo1/3a localization, expression of Eos and signaling via Neuropilin-1. Additional studies may help to define approaches that can undermine T(reg) stability in cancer or enhance T(reg) stability in transplantation, autoimmune or inflammatory diseases and therefore have substantial therapeutic utility. In this review, we will discuss how T(reg) stability is defined and the mechanisms utilized to maintain stability.
MeSH term(s)	Animals ; Epigenesis, Genetic ; Forkhead Transcription Factors/immunology ; Humans ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	FOXP3 protein, human ; Forkhead Transcription Factors
Language	English
Publishing date	2016-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2015.12.009
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Zs.A 2773: 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: Treg Fragility: A Prerequisite for Effective Antitumor Immunity?

Overacre-Delgoffe, Abigail E / Vignali, Dario A A

Cancer immunology research

2018 Volume 6, Issue 8, Page(s) 882–887

Abstract: Inhibitory checkpoint blockade has significantly improved patient response rate across numerous tumor types. However, most patients remain unresponsive to immunotherapy, suggesting that unappreciated mechanisms of resistance exist. The tumor ... ...

Abstract	Inhibitory checkpoint blockade has significantly improved patient response rate across numerous tumor types. However, most patients remain unresponsive to immunotherapy, suggesting that unappreciated mechanisms of resistance exist. The tumor microenvironment (TME) is unique and composed of many suppressive cell populations that inhibit antitumor immune responses, including regulatory T cells (Tregs). The TME is nutrient poor, acidic, and hypoxic, creating a challenging microenvironment for immune cells to function and survive. Tregs suppress a wide variety of cell populations through multiple mechanisms and are tasked with limiting tissue damage. Tregs are now considered to be a barrier to effective antitumor immunity. Systemic Treg depletion is not favored because of their critical role in maintaining immune homeostasis and preventing autoimmunity. Reducing Treg function specifically within the TME may provide a more effective, targeted approach to limit the immunosuppressive environment within the tumor without inducing systemic adverse consequences. Targeting molecules that cause Treg instability, characterized by loss of critical Treg transcription factors such as Foxp3, could result in conversion into cells that cause immune pathology, tissue damage, and subsequent autoimmune side effects. Interferon-γ (IFNγ) can cause intratumoral Treg "fragility," which results in loss of suppressive activity and increased IFNγ production without loss of Foxp3 expression and gross Treg "identity." We reviewed the impact Tregs have on the TME and vice versa, and their implications for responsiveness to cancer immunotherapy. We propose that the extent to which intratumoral Tregs develop a "fragile" phenotype following immunotherapy will predict and dictate responsiveness.
MeSH term(s)	Humans ; Immunotherapy/methods ; Neoplasms/immunology ; Neoplasms/therapy ; T-Lymphocytes, Regulatory/immunology ; Tumor Escape/immunology ; Tumor Microenvironment/immunology
Language	English
Publishing date	2018-08-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-18-0066
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Article ; Online: Microbiota-specific T follicular helper cells drive tertiary lymphoid structures and anti-tumor immunity against colorectal cancer.

Overacre-Delgoffe, Abigail E / Bumgarner, Hannah J / Cillo, Anthony R / Burr, Ansen H P / Tometich, Justin T / Bhattacharjee, Amrita / Bruno, Tullia C / Vignali, Dario A A / Hand, Timothy W

Immunity

2021 Volume 54, Issue 12, Page(s) 2812–2824.e4

Abstract: The composition of the intestinal microbiota is associated with both the development of tumors and the efficacy of anti-tumor immunity. Here, we examined the impact of microbiota-specific T cells in anti-colorectal cancer (CRC) immunity. Introduction of ... ...

Abstract	The composition of the intestinal microbiota is associated with both the development of tumors and the efficacy of anti-tumor immunity. Here, we examined the impact of microbiota-specific T cells in anti-colorectal cancer (CRC) immunity. Introduction of Helicobacter hepaticus (Hhep) in a mouse model of CRC did not alter the microbial landscape but increased tumor infiltration by cytotoxic lymphocytes and inhibited tumor growth. Anti-tumor immunity was independent of CD8
MeSH term(s)	Animals ; B-Lymphocyte Subsets/immunology ; CD4-Positive T-Lymphocytes/immunology ; Colon/pathology ; Colorectal Neoplasms/immunology ; Disease Models, Animal ; Gastrointestinal Microbiome/immunology ; Helicobacter Infections/immunology ; Helicobacter hepaticus/physiology ; Humans ; Killer Cells, Natural/immunology ; Lymphocytes, Tumor-Infiltrating/immunology ; Mice ; Proto-Oncogene Proteins c-bcl-6/genetics ; Proto-Oncogene Proteins c-bcl-6/metabolism ; T Follicular Helper Cells/immunology ; Tertiary Lymphoid Structures/immunology
Chemical Substances	Bcl6 protein, mouse ; Proto-Oncogene Proteins c-bcl-6
Language	English
Publishing date	2021-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2021.11.003
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Zs.A 4227: 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: Environmental enteric dysfunction induces regulatory T cells that inhibit local CD4+ T cell responses and impair oral vaccine efficacy.

Bhattacharjee, Amrita / Burr, Ansen H P / Overacre-Delgoffe, Abigail E / Tometich, Justin T / Yang, Deyi / Huckestein, Brydie R / Linehan, Jonathan L / Spencer, Sean P / Hall, Jason A / Harrison, Oliver J / Morais da Fonseca, Denise / Norton, Elizabeth B / Belkaid, Yasmine / Hand, Timothy W

Immunity

2021 Volume 54, Issue 8, Page(s) 1745–1757.e7

Abstract: ... dependent mouse EED model. Analysis of E. coli-labile toxin vaccine-specific CD4 ...

Abstract	Environmental enteric dysfunction (EED) is a gastrointestinal inflammatory disease caused by malnutrition and chronic infection. EED is associated with stunting in children and reduced efficacy of oral vaccines. To study the mechanisms of oral vaccine failure during EED, we developed a microbiota- and diet-dependent mouse EED model. Analysis of E. coli-labile toxin vaccine-specific CD4
MeSH term(s)	Administration, Oral ; Animals ; Bacterial Toxins/immunology ; Cell Line ; Disease Models, Animal ; Drosophila ; Escherichia coli/immunology ; Escherichia coli Vaccines/immunology ; Female ; Forkhead Transcription Factors/metabolism ; Gastrointestinal Diseases/immunology ; Gastrointestinal Diseases/microbiology ; Gastrointestinal Diseases/pathology ; Intestine, Small/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; T-Lymphocytes, Regulatory/immunology ; Vaccination
Chemical Substances	Bacterial Toxins ; Escherichia coli Vaccines ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Nuclear Receptor Subfamily 1, Group F, Member 3
Language	English
Publishing date	2021-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2021.07.005
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Zs.A 4227: 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: Metabolic support of tumour-infiltrating regulatory T cells by lactic acid.

Watson, McLane J / Vignali, Paolo D A / Mullett, Steven J / Overacre-Delgoffe, Abigail E / Peralta, Ronal M / Grebinoski, Stephanie / Menk, Ashley V / Rittenhouse, Natalie L / DePeaux, Kristin / Whetstone, Ryan D / Vignali, Dario A A / Hand, Timothy W / Poholek, Amanda C / Morrison, Brett M / Rothstein, Jeffrey D / Wendell, Stacy G / Delgoffe, Greg M

Nature

2021 Volume 591, Issue 7851, Page(s) 645–651

Abstract: Regulatory T ( ... ...

Abstract	Regulatory T (T
MeSH term(s)	Animals ; Cell Line, Tumor ; Cell Proliferation ; Female ; Glucose/metabolism ; Humans ; Lactic Acid/metabolism ; Lymphocytes, Tumor-Infiltrating/immunology ; Lymphocytes, Tumor-Infiltrating/metabolism ; Male ; Mice ; Neoplasms/immunology ; Suppressor Factors, Immunologic/immunology ; Suppressor Factors, Immunologic/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	Suppressor Factors, Immunologic ; Lactic Acid (33X04XA5AT) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-02-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-020-03045-2
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Zs.A 26: 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)
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Article ; Online: Considerations for treatment duration in responders to immune checkpoint inhibitors.

Marron, Thomas U / Ryan, Aideen E / Reddy, Sangeetha M / Kaczanowska, Sabina / Younis, Rania H / Thakkar, Dipti / Zhang, Jiajia / Bartkowiak, Todd / Howard, Rachel / Anderson, Kristin G / Olson, Daniel / Naqash, Abdul Rafeh / Patel, Ravi B / Sachdev, Esha / Rodriguez-Ruiz, Maria E / Sheffer, Michal / Church, Sarah / Fuhrman, Christopher / Overacre-Delgoffe, Abigail /

Nguyen, Rosa / Florou, Vaia / Thaxton, Jessica E / Aggen, David H / Guerriero, Jennifer L

Journal for immunotherapy of cancer

2021 Volume 9, Issue 3

Abstract: Immune checkpoint inhibitors (ICIs) have improved overall survival for cancer patients, however, optimal duration of ICI therapy has yet to be defined. Given ICIs were first used to treat patients with metastatic melanoma, a condition that at the time ... ...

Abstract	Immune checkpoint inhibitors (ICIs) have improved overall survival for cancer patients, however, optimal duration of ICI therapy has yet to be defined. Given ICIs were first used to treat patients with metastatic melanoma, a condition that at the time was incurable, little attention was initially paid to how much therapy would be needed for a durable response. As the early immunotherapy trials have matured past 10 years, a significant per cent of patients have demonstrated durable responses; it is now time to determine whether patients have been overtreated, and if durable remissions can still be achieved with less therapy, limiting the physical and financial toxicity associated with years of treatment. Well-designed trials are needed to identify optimal duration of therapy, and to define biomarkers to predict who would benefit from shorter courses of immunotherapy. Here, we outline key questions related to health, financial and societal toxicities of over treating with ICI and present four unique clinical trials aimed at exposing criteria for early cessation of ICI. Taken together, there is a serious liability to overtreating patients with ICI and future work is warranted to determine when it is safe to stop ICI.
MeSH term(s)	Clinical Trials as Topic ; Drug Administration Schedule ; Evidence-Based Medicine ; Humans ; Immune Checkpoint Inhibitors/administration & dosage ; Immune Checkpoint Inhibitors/adverse effects ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/mortality ; Neoplasms/pathology ; Patient Safety ; Risk Assessment ; Risk Factors ; Time Factors ; Treatment Outcome
Chemical Substances	Immune Checkpoint Inhibitors
Language	English
Publishing date	2021-03-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2020-001901
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Article ; Online: Prevalence of intratumoral regulatory T cells expressing neuropilin-1 is associated with poorer outcomes in patients with cancer.

Chuckran, Christopher A / Cillo, Anthony R / Moskovitz, Jessica / Overacre-Delgoffe, Abigail / Somasundaram, Ashwin S / Shan, Feng / Magnon, Grant C / Kunning, Sheryl R / Abecassis, Irina / Zureikat, Amer H / Luketich, James / Pennathur, Arjun / Sembrat, John / Rojas, Mauricio / Merrick, Daniel T / Taylor, Sarah E / Orr, Brian / Modugno, Francesmary / Buckanovich, Ron /

Schoen, Robert E / Kim, Seungwon / Duvvuri, Umamaheswar / Zeh, Herbert / Edwards, Robert / Kirkwood, John M / Coffman, Lan / Ferris, Robert L / Bruno, Tullia C / Vignali, Dario A A

Science translational medicine

2021 Volume 13, Issue 623, Page(s) eabf8495

Abstract: Despite the success of immune checkpoint blockade therapy, few strategies sufficiently overcome immunosuppression within the tumor microenvironment (TME). Targeting regulatory T cells ( ... ...

Abstract	Despite the success of immune checkpoint blockade therapy, few strategies sufficiently overcome immunosuppression within the tumor microenvironment (TME). Targeting regulatory T cells (T
MeSH term(s)	Animals ; Head and Neck Neoplasms ; Humans ; Immunotherapy ; Mice ; Neuropilin-1/metabolism ; Prevalence ; T-Lymphocytes, Regulatory ; Tumor Microenvironment
Chemical Substances	Neuropilin-1 (144713-63-3)
Language	English
Publishing date	2021-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abf8495
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