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Article ; Online: The Emerging Roles of Endoplasmic Reticulum Stress in Balancing Immunity and Tolerance in Health and Diseases: Mechanisms and Opportunities.

Li, Anqi / Song, No-Joon / Riesenberg, Brian P / Li, Zihai

2020 Volume 10, Page(s) 3154

Abstract: The endoplasmic reticulum (ER) is an organelle equipped with mechanisms for proper protein folding, trafficking, and degradation to maintain protein homeostasis in the secretory pathway. As a defense mechanism, perturbation of ER proteostasis by ER ... ...

Abstract	The endoplasmic reticulum (ER) is an organelle equipped with mechanisms for proper protein folding, trafficking, and degradation to maintain protein homeostasis in the secretory pathway. As a defense mechanism, perturbation of ER proteostasis by ER stress agents activates a cascade of signaling pathways from the ER to the nucleus known as unfolded protein response (UPR). The primary goal of UPR is to induce transcriptional and translational programs to restore ER homeostasis for cell survival. As such, defects in UPR signaling have been implicated as a key contributor to multiple diseases including metabolic diseases, degenerative diseases, inflammatory disorders, and cancer. Growing evidence support the critical role of ER stress in regulating the fate as well as the magnitude of the immune response. Moreover, the availability of multiple UPR pharmacological inhibitors raises the hope that targeting UPR can be a new strategy for immune modulation and immunotherapy of diseases. This paper reviews the principal mechanisms by which ER stress affects immune cell biology and function, with a focus of discussion on UPR-associated immunopathology and the development of potential ER stress-targeted therapeutics.
MeSH term(s)	Animals ; Endoplasmic Reticulum Stress/immunology ; Homeostasis/immunology ; Humans ; Immune Tolerance/immunology ; Immunity/immunology ; Unfolded Protein Response/immunology
Language	English
Publishing date	2020-02-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.03154
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: mRNA vaccines against SARS-CoV-2 induce divergent antigen-specific T-cell responses in patients with lung cancer.

Song, No-Joon / Chakravarthy, Karthik B / Jeon, Hyeongseon / Bolyard, Chelsea / Reynolds, Kelsi / Weller, Kevin P / Reisinger, Sarah / Wang, Yi / Li, Anqi / Jiang, Sizun / Ma, Qin / Barouch, Dan H / Rubinstein, Mark P / Shields, Peter G / Oltz, Eugene M / Chung, Dongjun / Li, Zihai

Journal for immunotherapy of cancer

2024 Volume 12, Issue 1

Abstract: Background: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant is highly transmissible and evades pre-established immunity. Messenger RNA (mRNA) vaccination against ancestral strain spike protein can induce intact T-cell ... ...

Abstract	Background: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant is highly transmissible and evades pre-established immunity. Messenger RNA (mRNA) vaccination against ancestral strain spike protein can induce intact T-cell immunity against the Omicron variant, but efficacy of booster vaccination in patients with late-stage lung cancer on immune-modulating agents including anti-programmed cell death protein 1(PD-1)/programmed death-ligand 1 (PD-L1) has not yet been elucidated. Methods: We assessed T-cell responses using a modified activation-induced marker assay, coupled with high-dimension flow cytometry analyses. Peripheral blood mononuclear cells (PBMCs) were stimulated with various viral peptides and antigen-specific T-cell responses were evaluated using flow cytometry. Results: Booster vaccines induced CD8 Conclusion: We conclude that patients with lung cancer on immunotherapy show a substantial qualitative deviation from non-cancer subjects in their T-cell response to mRNA vaccines, highlighting the need for heightened protective measures for patients with cancer to minimize the risk of breakthrough infection with the Omicron and other future variants.
MeSH term(s)	Humans ; Female ; mRNA Vaccines ; Lung Neoplasms ; COVID-19 Vaccines/therapeutic use ; SARS-CoV-2 ; Leukocytes, Mononuclear ; COVID-19/prevention & control
Chemical Substances	mRNA Vaccines ; COVID-19 Vaccines
Language	English
Publishing date	2024-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2023-007922
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Article: Development of molecular and pharmacological switches for chimeric antigen receptor T cells.

Wu, Bill X / Song, No-Joon / Riesenberg, Brian P / Li, Zihai

Experimental hematology & oncology

2019 Volume 8, Page(s) 27

Abstract: The use of chimeric antigen receptor (CAR) T cell technology as a therapeutic strategy for the treatment blood-born human cancers has delivered outstanding clinical efficacy. However, this treatment modality can also be associated with serious adverse ... ...

Abstract	The use of chimeric antigen receptor (CAR) T cell technology as a therapeutic strategy for the treatment blood-born human cancers has delivered outstanding clinical efficacy. However, this treatment modality can also be associated with serious adverse events in the form of cytokine release syndrome. While several avenues are being pursued to limit the off-target effects, it is critically important that any intervention strategy has minimal consequences on long term efficacy. A recent study published in Science Translational Medicine by Dr. Hudecek's group proved that dasatinib, a tyrosine kinase inhibitor, can serve as an on/off switch for CD19-CAR-T cells in preclinical models by limiting toxicities while maintaining therapeutic efficacy. In this editorial, we discuss the recent strategies for generating safer CAR-T cells, and also important questions surrounding the use of dasatinib for emergency intervention of CAR-T cell mediated cytokine release syndrome.
Language	English
Publishing date	2019-11-05
Publishing country	England
Document type	Editorial
ZDB-ID	2669066-4
ISSN	2162-3619
ISSN	2162-3619
DOI	10.1186/s40164-019-0151-z
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Article: Sesamol Increases Ucp1 Expression in White Adipose Tissues and Stimulates Energy Expenditure in High-Fat Diet-Fed Obese Mice

Lee, Dong Ho / Chang, Seo-Hyuk / Yang, Dong Kwon / Song, No-Joon / Yun, Ui Jeong / Park, Kye Won

Nutrients. 2020 May 18, v. 12, no. 5

2020

Abstract: Sesamol found in sesame oil has been shown to ameliorate obesity by regulating lipid metabolism. However, its effects on energy expenditure and the underlying molecular mechanism have not been clearly elucidated. In this study, we show that sesamol ... ...

Abstract	Sesamol found in sesame oil has been shown to ameliorate obesity by regulating lipid metabolism. However, its effects on energy expenditure and the underlying molecular mechanism have not been clearly elucidated. In this study, we show that sesamol increased the uncoupling protein 1 (Ucp1) expression in adipocytes. The administration of sesamol in high-fat diet (HFD)-fed mice prevented weight gain and improved metabolic derangements. The three-week sesamol treatment of HFD-fed mice, when the body weights were not different between the sesamol and control groups, increased energy expenditure, suggesting that an induced energy expenditure is a primary contributing factor for sesamol’s anti-obese effects. Consistently, sesamol induced the expression of energy-dissipating thermogenic genes, including Ucp1, in white adipose tissues. The microarray analysis showed that sesamol dramatically increased the Nrf2 target genes such as Hmox1 and Atf3 in adipocytes. Moreover, 76% (60/79 genes) of the sesamol-induced genes were also regulated by tert-butylhydroquinone (tBHQ), a known Nrf2 activator. We further verified that sesamol directly activated the Nrf2-mediated transcription. In addition, the Hmox1 and Ucp1 induction by sesamol was compromised in Nrf2-deleted cells, indicating the necessity of Nrf2 in the sesamol-mediated Ucp1 induction. Together, these findings demonstrate the effects of sesamol in inducing Ucp1 and in increasing energy expenditure, further highlighting the use of the Nrf2 activation in stimulating thermogenic adipocytes and in increasing energy expenditure in obesity and its related metabolic diseases.
Keywords	adipocytes ; energy expenditure ; genes ; high fat diet ; hydroquinone ; lipid metabolism ; metabolic diseases ; mice ; microarray technology ; nutrients ; obesity ; sesame oil ; weight gain
Language	English
Dates of publication	2020-0518
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-light
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12051459
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Sesamol Increases Ucp1 Expression in White Adipose Tissues and Stimulates Energy Expenditure in High-Fat Diet-Fed Obese Mice.

Lee, Dong Ho / Chang, Seo-Hyuk / Yang, Dong Kwon / Song, No-Joon / Yun, Ui Jeong / Park, Kye Won

Nutrients

2020 Volume 12, Issue 5

Abstract	Sesamol found in sesame oil has been shown to ameliorate obesity by regulating lipid metabolism. However, its effects on energy expenditure and the underlying molecular mechanism have not been clearly elucidated. In this study, we show that sesamol increased the uncoupling protein 1 (Ucp1) expression in adipocytes. The administration of sesamol in high-fat diet (HFD)-fed mice prevented weight gain and improved metabolic derangements. The three-week sesamol treatment of HFD-fed mice, when the body weights were not different between the sesamol and control groups, increased energy expenditure, suggesting that an induced energy expenditure is a primary contributing factor for sesamol's anti-obese effects. Consistently, sesamol induced the expression of energy-dissipating thermogenic genes, including
MeSH term(s)	Adipocytes/drug effects ; Adipose Tissue, White/metabolism ; Animals ; Benzodioxoles/pharmacology ; Cell Culture Techniques ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Energy Metabolism/drug effects ; Mice ; Mice, Obese ; Obesity/metabolism ; Phenols/pharmacology ; Uncoupling Protein 1/drug effects ; Weight Gain/drug effects
Chemical Substances	Benzodioxoles ; Phenols ; Ucp1 protein, mouse ; Uncoupling Protein 1 ; sesamol (94IEA0NV89)
Language	English
Publishing date	2020-05-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12051459
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Article ; Online: Epiregulin as an Alternative Ligand for Leptin Receptor Alleviates Glucose Intolerance without Change in Obesity

No-Joon Song / Aejin Lee / Rumana Yasmeen / Qiwen Shen / Kefeng Yang / Shashi Bhushan Kumar / Danah Muhanna / Shanvanth Arnipalli / Sabrena F. Noria / Bradley J. Needleman / Jeffrey W. Hazey / Dean J. Mikami / Joana Ortega-Anaya / Rafael Jiménez-Flores / Jeremy Prokop / Ouliana Ziouzenkova

Cells, Vol 11, Iss 425, p

2022 Volume 425

Abstract: The leptin receptor (LepR) acts as a signaling nexus for the regulation of glucose uptake and obesity, among other metabolic responses. The functional role of LepR under leptin-deficient conditions remains unclear. This study reports that epiregulin ( ... ...

Abstract	The leptin receptor (LepR) acts as a signaling nexus for the regulation of glucose uptake and obesity, among other metabolic responses. The functional role of LepR under leptin-deficient conditions remains unclear. This study reports that epiregulin (EREG) governed glucose uptake in vitro and in vivo in Lep ob mice by activating LepR under leptin-deficient conditions. Single and long-term treatment with EREG effectively rescued glucose intolerance in comparative insulin and EREG tolerance tests in Lep ob mice. The immunoprecipitation study revealed binding between EREG and LepR in adipose tissue of Lep ob mice. EREG/LepR regulated glucose uptake without changes in obesity in Lep ob mice via mechanisms, including ERK activation and translocation of GLUT4 to the cell surface. EREG-dependent glucose uptake was abolished in Lepr db mice which supports a key role of LepR in this process. In contrast, inhibition of the canonical epidermal growth factor receptor (EGFR) pathway implicated in other EREG responses, increased glucose uptake. Our data provide a basis for understanding glycemic responses of EREG that are dependent on LepR unlike functions mediated by EGFR, including leptin secretion, thermogenesis, pain, growth, and other responses. The computational analysis identified a conserved amino acid sequence, supporting an evolutionary role of EREG as an alternative LepR ligand.
Keywords	epiregulin ; leptin receptor ; ERK ; EGFR ; glucose uptake ; energy metabolism ; Biology (General) ; QH301-705.5
Subject code	570 ; 333
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mechanisms underlying UCP1 dependent and independent adipocyte thermogenesis.

Chang, Seo-Hyuk / Song, No-Joon / Choi, Jin Hee / Yun, Ui Jeong / Park, Kye Won

Obesity reviews : an official journal of the International Association for the Study of Obesity

2018 Volume 20, Issue 2, Page(s) 241–251

Abstract: The growing focus on brown adipocytes has spurred an interest in their potential benefits for metabolic diseases. Brown and beige (or brite) adipocytes express high levels of uncoupling protein 1 (Ucp1) to dissipate heat instead of generating ATP. Ucp1 ... ...

Abstract	The growing focus on brown adipocytes has spurred an interest in their potential benefits for metabolic diseases. Brown and beige (or brite) adipocytes express high levels of uncoupling protein 1 (Ucp1) to dissipate heat instead of generating ATP. Ucp1 induction by stimuli including cold, exercise, and diet increases nonshivering thermogenesis, leading to increased energy expenditure and prevention of obesity. Recently, studies in adipocytes have indicated the existence of functional Ucp1-independent thermogenic regulators. Furthermore, substrate cycling involving creatine metabolites, cold-induced N-acyl amino acids, and oxidized lipids in white adipocytes can increase energy expenditure in the absence of Ucp1. These studies emphasize the need for a better understanding of the mechanisms governing energy expenditure in adipocytes and their potential applications in the prevention of human obesity and metabolic diseases.
MeSH term(s)	Adipocytes/metabolism ; Animals ; Energy Metabolism/physiology ; Humans ; Mitochondria/metabolism ; Thermogenesis/physiology ; Uncoupling Protein 1/metabolism
Chemical Substances	Uncoupling Protein 1
Language	English
Publishing date	2018-11-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2147980-X
ISSN	1467-789X ; 1467-7881
ISSN (online)	1467-789X
ISSN	1467-7881
DOI	10.1111/obr.12796
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Article ; Online: Butein-Enriched Fractions of

Jang, Jaeyool / Chang, Seo-Hyuk / Song, Dawoon / Song, No-Joon / Han, Saeroarum / Oh, Seungjun / Yun, Ui Jeong / Ahn, Jee-Yin / Lee, Sukchan / Ku, Jin-Mo / Park, Kye Won

Journal of medicinal food

2021 Volume 24, Issue 12, Page(s) 1271–1279

Abstract: ... Butea ... ...

Abstract	Butea monosperma
MeSH term(s)	Animals ; Butea/chemistry ; Chalcones/pharmacology ; Diet, High-Fat/adverse effects ; Energy Metabolism ; Fibroblasts ; Flowers/chemistry ; Mice ; Mice, Obese ; Plant Extracts/pharmacology ; Weight Gain
Chemical Substances	Chalcones ; Plant Extracts ; butein (4WVS5M0LGF)
Language	English
Publishing date	2021-11-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	1427365-2
ISSN	1557-7600 ; 1096-620X
ISSN (online)	1557-7600
ISSN	1096-620X
DOI	10.1089/jmf.2021.K.0074
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Article: Mechanisms underlying UCP1 dependent and independent adipocyte thermogenesis

Chang, Seo‐Hyuk / Jin Hee Choi / Kye Won Park / No‐Joon Song / Ui Jeong Yun

Obesity reviews. 2019 Feb., v. 20, no. 2

2019

Abstract	The growing focus on brown adipocytes has spurred an interest in their potential benefits for metabolic diseases. Brown and beige (or brite) adipocytes express high levels of uncoupling protein 1 (Ucp1) to dissipate heat instead of generating ATP. Ucp1 induction by stimuli including cold, exercise, and diet increases nonshivering thermogenesis, leading to increased energy expenditure and prevention of obesity. Recently, studies in adipocytes have indicated the existence of functional Ucp1‐independent thermogenic regulators. Furthermore, substrate cycling involving creatine metabolites, cold‐induced N‐acyl amino acids, and oxidized lipids in white adipocytes can increase energy expenditure in the absence of Ucp1. These studies emphasize the need for a better understanding of the mechanisms governing energy expenditure in adipocytes and their potential applications in the prevention of human obesity and metabolic diseases.
Keywords	adenosine triphosphate ; amino acids ; brown adipocytes ; cold ; creatine ; diet ; energy expenditure ; exercise ; heat production ; lipids ; metabolic diseases ; metabolites ; obesity ; oxidation ; white adipocytes
Language	English
Dates of publication	2019-02
Size	p. 241-251.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	2147980-X
ISSN	1467-789X ; 1467-7881
ISSN (online)	1467-789X
ISSN	1467-7881
DOI	10.1111/obr.12796
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Article ; Online: Post-infusion PD-1+CD8+CAR-T cells identify patients responsive to CD19-CAR-T therapy in non-Hodgkin's lymphoma.

Denlinger, Nathan / Song, No-Joon / Zhang, Xiaoli / Jeon, Hyeongseon / Peterson, Chelsea / Wang, Yi / Reynolds, Kelsi / Bolz, Robert / Miao, Jessica / Song, Chunhua / Wu, Dayong / Chan, Wing Keung / Bezerra, Evandro D / Epperla, Narendranath / Voorhees, Timothy J / Brammer, Jonathan E / Kittai, Adam S / Bond, David A / Sawalha, Yazeed /

Sigmund, Audrey M / Reneau, John C / Rubinstein, Mark P / Hanel, Walter / Christian, Beth / Baiocchi, Robert A / Maddocks, Kami J / Alinari, Lapo / Vasu, Sumithira / de Lima, Marcos / Chung, Dongjun / Jaglowski, Samantha M / Li, Zihai / Huang, Xiaopei / Yang, Yiping

Blood advances

2024

Abstract: Chimeric antigen receptor T cell therapy (CAR-T) has revolutionized treatment for relapsed/refractory (r/r) B-cell non-Hodgkin's lymphoma (NHL). Robust biomarkers and a complete understanding of CAR-T cell function in the post-infusion phase remain ... ...

Abstract	Chimeric antigen receptor T cell therapy (CAR-T) has revolutionized treatment for relapsed/refractory (r/r) B-cell non-Hodgkin's lymphoma (NHL). Robust biomarkers and a complete understanding of CAR-T cell function in the post-infusion phase remain limited. Here we used a 37-color spectral flow cytometry panel to perform high dimensional single cell analysis of post-infusion samples in 26 patients treated with CD28 co-stimulatory domain containing commercial CAR-T (CD28-CAR-T) for NHL and focused on computationally gated CD8+ CAR-T cells. We found that the presence of post-infusion PD-1+ CD8+ CAR-T cells at the Day 14 timepoint highly correlated with the ability to achieve complete response (CR) by 6 months. Further analysis identified multiple subtypes of CD8+ PD-1+ CAR-T cells including PD-1+ TCF1+ stem-like CAR-T cells and PD-1+ TIM3+ effector-like CAR-T cells that correlated with improved clinical outcomes such as response and progression free survival. Additionally, we identified a subset of PD-1+ CD8+ CAR+ T cells with effector-like function that was increased in patients who achieved a CR and was associated with Grade 3 or higher immune effector cell-associated neurotoxicity syndrome. Here we identified robust biomarkers of response to CD28-CAR-T and highlight the importance of PD-1 positivity in CD8+ CAR-T cells post-infusion in achieving CR.
Language	English
Publishing date	2024-03-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023012073
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