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Article ; Online: What Lessons Can Radiologists Learn From the Holocaust Reparations Movement?

Eizenstat, Stuart E / Weisberg, Edmund M / Rowe, Steven P / Fishman, Elliot K / Chu, Linda C

Current problems in diagnostic radiology

2023 Volume 52, Issue 4, Page(s) 237–238

MeSH term(s)	Humans ; Holocaust ; Radiologists ; Physicians
Language	English
Publishing date	2023-03-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	198954-6
ISSN	1535-6302 ; 0363-0188
ISSN (online)	1535-6302
ISSN	0363-0188
DOI	10.1067/j.cpradiol.2023.03.014
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Article ; Online: Tissue-specific immunity for a changing world.

Weisberg, Stuart P / Ural, Basak B / Farber, Donna L

Cell

2021 Volume 184, Issue 6, Page(s) 1517–1529

Abstract: Our immune system has evolved to protect us from pathogens and maintain homeostasis through localization in diverse tissue sites throughout the body. Immune responses are orchestrated by T cells, which direct pathogen clearance at the infection site and ... ...

Abstract	Our immune system has evolved to protect us from pathogens and maintain homeostasis through localization in diverse tissue sites throughout the body. Immune responses are orchestrated by T cells, which direct pathogen clearance at the infection site and establish tissue-resident memory T cells (TRMs) for protection immunity. Here, we discuss how tissue immune responses are influenced by various stressors (e.g., metabolic, environmental, aging) that are rapidly changing due to climate fluctuations and globalization. We propose potential strategies for targeting tissue immunity to mitigate future pathogenic and environmental challenges and areas of investigation that can elucidate mechanisms for adapting and restoring homeostasis.
MeSH term(s)	Aging/immunology ; Animals ; Environment ; Humans ; Immune System/physiology ; Immunity ; Organ Specificity/immunology ; T-Lymphocytes/immunology
Language	English
Publishing date	2021-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2021.01.042
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Article: Societal change to prevent obesity.

Weisberg, Stuart P

JAMA

2002 Volume 288, Issue 17, Page(s) 2176

MeSH term(s)	Health Behavior ; Humans ; Obesity/epidemiology ; Obesity/prevention & control ; Social Change ; United States/epidemiology
Language	English
Publishing date	2002-11-06
Publishing country	United States
Document type	Editorial
ZDB-ID	2958-0
ISSN	1538-3598 ; 0098-7484 ; 0254-9077 ; 0002-9955
ISSN (online)	1538-3598
ISSN	0098-7484 ; 0254-9077 ; 0002-9955
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Article ; Online: Combination immunotherapy including OncoVEX

Gartrell, Robyn D / Blake, Zoë / Rizk, Emanuelle M / Perez-Lorenzo, Rolando / Weisberg, Stuart P / Simoes, Ines / Esancy, Camden / Fu, Yichun / Davari, Danielle R / Barker, Luke / Finkel, Grace / Mondal, Manas / Minns, Hanna E / Wang, Samuel W / Fullerton, Benjamin T / Lozano, Francisco / Chiuzan, Codruta / Horst, Basil / Saenger, Yvonne M

Cancer immunology, immunotherapy : CII

2022 Volume 71, Issue 8, Page(s) 1837–1849

Abstract: Talimogene Laherparepvec ( ... ...

Abstract	Talimogene Laherparepvec (OncoVEX
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Immunologic Factors/therapeutic use ; Immunotherapy ; Melanoma/drug therapy ; Mice ; Oncolytic Virotherapy ; Oncolytic Viruses ; Proto-Oncogene Proteins B-raf/genetics ; Tumor Microenvironment
Chemical Substances	Antineoplastic Agents ; Immunologic Factors ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2022-01-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-021-03088-y
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Article ; Online: Rapid and Flexible Platform To Assess Anti-SARS-CoV-2 Antibody Neutralization and Spike Protein-Specific Antivirals.

Stelitano, Debora / Weisberg, Stuart P / Goldklang, Monica P / Zhu, Yun / Bovier, Francesca T / Kalantarov, Gavreel F / Greco, Giuseppe / Decimo, Didier / Franci, Gianluigi / Cennamo, Michele / Portella, Giuseppe / Galdiero, Massimiliano / Mathieu, Cyrille / Horvat, Branka / Trakht, Ilya N / Moscona, Anne / Whitt, Michael A / Porotto, Matteo

mSphere

2021 Volume 6, Issue 4, Page(s) e0057121

Abstract: The COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is ongoing and has shown the community that flexible methods for rapidly identifying and screening candidate antivirals are needed. Assessing virus- ... ...

Abstract	The COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is ongoing and has shown the community that flexible methods for rapidly identifying and screening candidate antivirals are needed. Assessing virus-neutralizing activity of human serum to monitor population immunity and response to infection and vaccination is key to pandemic control. We developed a virus neutralization platform strategy that relies only on bioinformatic and genetic information of the virus of interest. The platform uses viral envelope glycoprotein cDNAs to set up an assay that mimics multicycle infection but is safe and, therefore, amenable to biosafety level 2 (BSL2) conditions for viruses that require BSL3 facilities (e.g., SARS-CoV-1 and SARS-CoV-2). As a complement to this platform, we present a new cell-based immunofluorescent (CBI) assay that uses SARS-CoV-2 spike protein (S)-expressing cells to accurately measure the neutralization potential of human sera and is readily adaptable to variants of concern. These methods should be useful additions to the tools for assessing antiviral immunity, whether acquired via natural infection or vaccines.
MeSH term(s)	Animals ; Antibodies, Neutralizing/immunology ; Antibodies, Viral/immunology ; Antiviral Agents/immunology ; COVID-19/immunology ; COVID-19/virology ; Cell Line ; Chlorocebus aethiops ; HEK293 Cells ; Humans ; Neutralization Tests/methods ; Pandemics/prevention & control ; SARS-CoV-2/immunology ; Spike Glycoprotein, Coronavirus/immunology ; Vero Cells
Chemical Substances	Antibodies, Neutralizing ; Antibodies, Viral ; Antiviral Agents ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-5042
ISSN (online)	2379-5042
DOI	10.1128/mSphere.00571-21
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Article ; Online: Immune and epithelial determinants of age-related risk and alveolar injury in fatal COVID-19.

Chait, Michael / Yilmaz, Mine M / Shakil, Shanila / Ku, Amy W / Dogra, Pranay / Connors, Thomas J / Szabo, Peter A / Gray, Joshua I / Wells, Steven B / Kubota, Masaru / Matsumoto, Rei / Poon, Maya Ml / Snyder, Mark E / Baldwin, Matthew R / Sims, Peter A / Saqi, Anjali / Farber, Donna L / Weisberg, Stuart P

JCI insight

2022 Volume 7, Issue 11

Abstract: Respiratory failure in COVID-19 is characterized by widespread disruption of the lung's alveolar gas exchange interface. To elucidate determinants of alveolar lung damage, we performed epithelial and immune cell profiling in lungs from 24 COVID-19 ... ...

Abstract	Respiratory failure in COVID-19 is characterized by widespread disruption of the lung's alveolar gas exchange interface. To elucidate determinants of alveolar lung damage, we performed epithelial and immune cell profiling in lungs from 24 COVID-19 autopsies and 43 uninfected organ donors ages 18-92 years. We found marked loss of type 2 alveolar epithelial (T2AE) cells and increased perialveolar lymphocyte cytotoxicity in all fatal COVID-19 cases, even at early stages before typical patterns of acute lung injury are histologically apparent. In lungs from uninfected organ donors, there was also progressive loss of T2AE cells with increasing age, which may increase susceptibility to COVID-19-mediated lung damage in older individuals. In the fatal COVID-19 cases, macrophage infiltration differed according to the histopathological pattern of lung injury. In cases with acute lung injury, we found accumulation of CD4+ macrophages that expressed distinctly high levels of T cell activation and costimulation genes and strongly correlated with increased extent of alveolar epithelial cell depletion and CD8+ T cell cytotoxicity. Together, our results show that T2AE cell deficiency may underlie age-related COVID-19 risk and initiate alveolar dysfunction shortly after infection, and we define immune cell mediators that may contribute to alveolar injury in distinct pathological stages of fatal COVID-19.
MeSH term(s)	Acute Lung Injury/pathology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Alveolar Epithelial Cells/pathology ; Autopsy ; COVID-19 ; Humans ; Lung/pathology ; Middle Aged ; Young Adult
Language	English
Publishing date	2022-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.157608
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Article ; Online: Increased erythrophagocytosis induces ferroptosis in red pulp macrophages in a mouse model of transfusion.

Youssef, Lyla A / Rebbaa, Abdelhadi / Pampou, Sergey / Weisberg, Stuart P / Stockwell, Brent R / Hod, Eldad A / Spitalnik, Steven L

Blood

2018 Volume 131, Issue 23, Page(s) 2581–2593

Abstract: Macrophages play important roles in recycling iron derived from the clearance of red blood cells (RBCs). They are also a critically important component of host defense, protecting against invading pathogens. However, the effects on macrophage biology of ... ...

Abstract	Macrophages play important roles in recycling iron derived from the clearance of red blood cells (RBCs). They are also a critically important component of host defense, protecting against invading pathogens. However, the effects on macrophage biology of acutely ingesting large numbers of RBCs are not completely understood. To investigate this issue, we used a mouse model of RBC transfusion and clearance, which mimics the clinical setting. In this model, transfusions of refrigerator storage-damaged (ie, "old") RBCs led to increased erythrophagocytosis by splenic red pulp macrophages (RPMs). This robust erythrophagocytosis induced ferroptosis, an iron-dependent form of cell death, in RPMs. This was accompanied by increases in reactive oxygen species and lipid peroxidation in vivo, which were reduced by treatment in vitro with ferrostatin-1, a ferroptosis inhibitor. Old RBC transfusions also induced RPM-dependent chemokine expression by splenic Ly6C
MeSH term(s)	Animals ; Cell Death ; Cell Division ; Disease Models, Animal ; Erythrocyte Transfusion/adverse effects ; Erythrocytes/cytology ; Erythrocytes/immunology ; Lipid Peroxidation ; Macrophages/cytology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology ; Monocytes/immunology ; Phagocytosis
Language	English
Publishing date	2018-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2017-12-822619
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Article ; Online: An apparent role for Alox15 in the pathogenesis of diabetes in the NOD mouse: parsing the supporting genetic data.

Weisberg, Stuart P / Leibel, Rudolph L

Diabetes

2008 Volume 57, Issue 1, Page(s) 1–2

MeSH term(s)	Animals ; Arachidonate 12-Lipoxygenase/deficiency ; Arachidonate 12-Lipoxygenase/genetics ; Arachidonate 15-Lipoxygenase/deficiency ; Arachidonate 15-Lipoxygenase/genetics ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 1/prevention & control ; Disease Models, Animal ; Humans ; Insulin-Secreting Cells/pathology ; Mice ; Mice, Inbred NOD/genetics ; Multienzyme Complexes/deficiency ; Multienzyme Complexes/genetics
Chemical Substances	Multienzyme Complexes ; Alox15 protein, mouse (EC 1.13.11.31) ; Arachidonate 12-Lipoxygenase (EC 1.13.11.31) ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33)
Language	English
Publishing date	2008-01
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db07-1592
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Article ; Online: Immune cells and their inflammatory mediators modify β cells and cause checkpoint inhibitor-induced diabetes.

JCI insight

2022 Volume 7, Issue 17

Abstract: Checkpoint inhibitors (CPIs) targeting programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) have revolutionized cancer treatment but can trigger autoimmune complications, including CPI-induced diabetes ...

Abstract	Checkpoint inhibitors (CPIs) targeting programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) have revolutionized cancer treatment but can trigger autoimmune complications, including CPI-induced diabetes mellitus (CPI-DM), which occurs preferentially with PD-1 blockade. We found evidence of pancreatic inflammation in patients with CPI-DM with shrinkage of pancreases, increased pancreatic enzymes, and in a case from a patient who died with CPI-DM, peri-islet lymphocytic infiltration. In the NOD mouse model, anti-PD-L1 but not anti-CTLA-4 induced diabetes rapidly. RNA sequencing revealed that cytolytic IFN-γ+CD8+ T cells infiltrated islets with anti-PD-L1. Changes in β cells were predominantly driven by IFN-γ and TNF-α and included induction of a potentially novel β cell population with transcriptional changes suggesting dedifferentiation. IFN-γ increased checkpoint ligand expression and activated apoptosis pathways in human β cells in vitro. Treatment with anti-IFN-γ and anti-TNF-α prevented CPI-DM in anti-PD-L1-treated NOD mice. CPIs targeting the PD-1/PD-L1 pathway resulted in transcriptional changes in β cells and immune infiltrates that may lead to the development of diabetes. Inhibition of inflammatory cytokines can prevent CPI-DM, suggesting a strategy for clinical application to prevent this complication.
MeSH term(s)	Animals ; Diabetes Mellitus ; Humans ; Inflammation Mediators ; Mice ; Mice, Inbred NOD ; Programmed Cell Death 1 Receptor ; Tumor Necrosis Factor Inhibitors
Chemical Substances	Inflammation Mediators ; Programmed Cell Death 1 Receptor ; Tumor Necrosis Factor Inhibitors
Language	English
Publishing date	2022-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.156330
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Article ; Online: PAS-C platelets contain less plasma protein, lower anti-A and anti-B titers, and decreased HLA antibody specificities compared to plasma platelets.

Weisberg, Stuart P / Shaz, Beth H / Tumer, Gizem / Silliman, Chris C / Kelher, Marguerite R / Cohn, Claudia S

Transfusion

2018 Volume 58, Issue 4, Page(s) 891–895

Abstract: Background: Platelets (PLTs) collected and stored in PLT additive solution Intersol (PAS-C) are presumed to reduce recipient exposure to donor plasma components; however, the effects of PAS-C on PLT supernatant composition are poorly defined. Therefore, ...

Abstract	Background: Platelets (PLTs) collected and stored in PLT additive solution Intersol (PAS-C) are presumed to reduce recipient exposure to donor plasma components; however, the effects of PAS-C on PLT supernatant composition are poorly defined. Therefore, we compared the total protein concentration, isohemagglutinin titers, and HLA antibodies in supernatants of PAS-C PLTs to plasma PLTs. Study design and methods: Apheresis PLTs from group O blood donors were collected into either 100% donor plasma (n = 50) or a mixture of 65% PAS-C/35% donor plasma (n = 50). Within 12 hours of collection, samples of the PLT supernatant were frozen and stored. PLT supernatants were assayed for total protein concentration and anti-A and anti-B titers and screened for HLA antibodies. Samples positive for HLA antibodies were further tested using single-antigen bead assays to determine antibody strength and specificity. Results: Supernatants of PAS-C PLTs had significantly lower total protein concentration and anti-A and anti-B titers compared to plasma PLTs. There was no significant difference in the number of HLA antibody screen-positive PAS-C (3/50) compared to plasma PLT supernatants (2/50); however, the HLA antibody screen-positive supernatants of PAS-C PLTs had fewer HLA specificities (2) compared to those of the plasma PLTs (18). Conclusion: Decreased plasma proteins likely underlie lower rates of allergic and febrile, nonhemolytic transfusion reactions from the infusion of PAS-C PLTs. Decreased anti-A and anti-B titers may prevent hemolysis from minor ABO mismatch. Lower HLA antibody specificities may mitigate transfusion-related acute lung injury.
MeSH term(s)	ABO Blood-Group System/immunology ; Antibody Affinity ; Antibody Specificity ; Blood Group Incompatibility/prevention & control ; Blood Platelets/chemistry ; Blood Platelets/drug effects ; Blood Platelets/immunology ; Blood Preservation/methods ; Blood Proteins/analysis ; Epitopes/immunology ; Female ; HLA Antigens/immunology ; Hemagglutinins/blood ; Histocompatibility Testing/methods ; Humans ; Isoantibodies/blood ; Male ; Organ Preservation Solutions/pharmacology ; Plasma ; Plateletpheresis ; Transfusion-Related Acute Lung Injury/prevention & control
Chemical Substances	ABO Blood-Group System ; Blood Proteins ; Epitopes ; HLA Antigens ; Hemagglutinins ; Isoantibodies ; Organ Preservation Solutions
Language	English
Publishing date	2018-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208417-x
ISSN	1537-2995 ; 0041-1132
ISSN (online)	1537-2995
ISSN	0041-1132
DOI	10.1111/trf.14523
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