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Article ; Online: Immunotherapy partners after progression: Right place, right time?

Rouhani, Sherin J / Bestvina, Christine M

2022 Volume 129, Issue 2, Page(s) 181–183

MeSH term(s)	Humans ; Immunotherapy
Language	English
Publishing date	2022-11-24
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1429-1
ISSN	1097-0142 ; 0008-543X ; 1934-662X
ISSN (online)	1097-0142
ISSN	0008-543X ; 1934-662X
DOI	10.1002/cncr.34558
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Article ; Online: Effects of immune-related adverse events (irAEs) and their treatment on antitumor immune responses.

Blum, Steven M / Rouhani, Sherin J / Sullivan, Ryan J

Immunological reviews

2023 Volume 318, Issue 1, Page(s) 167–178

Abstract: Immune checkpoint inhibitors (ICIs) are potentially life-saving cancer therapies that can trigger immune-related adverse events (irAEs). irAEs can impact any organ and range in their presentation from mild side effects to life-threatening complications. ... ...

Abstract	Immune checkpoint inhibitors (ICIs) are potentially life-saving cancer therapies that can trigger immune-related adverse events (irAEs). irAEs can impact any organ and range in their presentation from mild side effects to life-threatening complications. The relationship between irAEs and antitumor immune responses is nuanced and may depend on the irAE organ, the tumor histology, and the patient. While some irAEs likely represent an immune response against antigens shared between tumor cells and healthy tissues, other irAEs may be entirely unrelated to antitumor immune responses. Clinical observations suggest that low-grade irAEs have a positive association with responses to ICIs, but the correlation between severe irAEs and clinical benefit is less clear. Currently, severe irAEs are typically treated by interrupting or permanently discontinuing ICI treatment and administering empirically selected systemic immunosuppressive agents. However, these interventions could potentially diminish the antitumor effects of ICIs. Efforts to understand the mechanistic relationship between irAEs and the tumor microenvironment have yielded meaningful insights and nominated therapeutic targets for irAE management that may preserve or even boost ICI efficacy. We explore the clinical and molecular relationship between irAEs and antitumor immunity as well as the role that irAE treatments may play in shaping antitumor immune responses.
MeSH term(s)	Humans ; Neoplasms/drug therapy ; Neoplasms/pathology ; Drug-Related Side Effects and Adverse Reactions ; Immune Checkpoint Inhibitors/adverse effects ; Immunity ; Tumor Microenvironment
Chemical Substances	Immune Checkpoint Inhibitors
Language	English
Publishing date	2023-08-14
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13262
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Article ; Online: Effects of immune‐related adverse events (irAEs) and their treatment on antitumor immune responses

Blum, Steven M. / Rouhani, Sherin J. / Sullivan, Ryan J.

Immunological Reviews. 2023 Sept., v. 318, no. 1 p.167-178

2023

Abstract: Immune checkpoint inhibitors (ICIs) are potentially life‐saving cancer therapies that can trigger immune‐related adverse events (irAEs). irAEs can impact any organ and range in their presentation from mild side effects to life‐threatening complications. ... ...

Abstract	Immune checkpoint inhibitors (ICIs) are potentially life‐saving cancer therapies that can trigger immune‐related adverse events (irAEs). irAEs can impact any organ and range in their presentation from mild side effects to life‐threatening complications. The relationship between irAEs and antitumor immune responses is nuanced and may depend on the irAE organ, the tumor histology, and the patient. While some irAEs likely represent an immune response against antigens shared between tumor cells and healthy tissues, other irAEs may be entirely unrelated to antitumor immune responses. Clinical observations suggest that low‐grade irAEs have a positive association with responses to ICIs, but the correlation between severe irAEs and clinical benefit is less clear. Currently, severe irAEs are typically treated by interrupting or permanently discontinuing ICI treatment and administering empirically selected systemic immunosuppressive agents. However, these interventions could potentially diminish the antitumor effects of ICIs. Efforts to understand the mechanistic relationship between irAEs and the tumor microenvironment have yielded meaningful insights and nominated therapeutic targets for irAE management that may preserve or even boost ICI efficacy. We explore the clinical and molecular relationship between irAEs and antitumor immunity as well as the role that irAE treatments may play in shaping antitumor immune responses.
Keywords	histology ; immune response ; immunosuppression ; neoplasms ; patients ; therapeutics
Language	English
Dates of publication	2023-09
Size	p. 167-178.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	REVIEW
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13262
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Article ; Online: Brief Report: Discordance Between Liquid and Tissue Biopsy-Based Next-Generation Sequencing in Lung Adenocarcinoma at Disease Progression.

Tran, Misha C / Strohbehn, Garth W / Karrison, Theodore G / Rouhani, Sherin J / Segal, Jeremy P / Shergill, Ardaman / Hoffman, Philip C / Patel, Jyoti D / Garassino, Marina C / Vokes, Everett E / Bestvina, Christine M

Clinical lung cancer

2023 Volume 24, Issue 3, Page(s) e117–e121

MeSH term(s)	Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Adenocarcinoma of Lung/genetics ; Biopsy ; Disease Progression ; High-Throughput Nucleotide Sequencing ; Biomarkers, Tumor ; Mutation
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2023-01-25
Publishing country	United States
Document type	Case Reports
ZDB-ID	2145146-1
ISSN	1938-0690 ; 1525-7304
ISSN (online)	1938-0690
ISSN	1525-7304
DOI	10.1016/j.cllc.2023.01.003
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Zs.A 5893: 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: Checkpoint Blockade-Induced Dermatitis and Colitis Are Dominated by Tissue-Resident Memory T Cells and Th1/Tc1 Cytokines.

Reschke, Robin / Shapiro, Jason W / Yu, Jovian / Rouhani, Sherin J / Olson, Daniel J / Zha, Yuanyuan / Gajewski, Thomas F

Cancer immunology research

2022 Volume 10, Issue 10, Page(s) 1167–1174

Abstract: Immune checkpoint blockade is therapeutically successful for many patients across multiple cancer types. However, immune-related adverse events (irAE) frequently occur and can sometimes be life threatening. It is critical to understand the immunologic ... ...

Abstract	Immune checkpoint blockade is therapeutically successful for many patients across multiple cancer types. However, immune-related adverse events (irAE) frequently occur and can sometimes be life threatening. It is critical to understand the immunologic mechanisms of irAEs with the goal of finding novel treatment targets. Herein, we report our analysis of tissues from patients with irAE dermatitis using multiparameter immunofluorescence (IF), spatial transcriptomics, and RNA in situ hybridization (RISH). Skin psoriasis cases were studied as a comparison, as a known Th17-driven disease, and colitis was investigated as a comparison. IF analysis revealed that CD4+ and CD8+ tissue-resident memory T (TRM) cells were preferentially expanded in the inflamed portion of skin in cutaneous irAEs compared with healthy skin controls. Spatial transcriptomics allowed us to focus on areas containing TRM cells to discern functional phenotype and revealed expression of Th1-associated genes in irAEs, compared with Th17-asociated genes in psoriasis. Expression of PD-1, CTLA-4, LAG-3, and other inhibitory receptors was observed in irAE cases. RISH technology combined with IF confirmed expression of IFNγ, CXCL9, CXCL10, and TNFα in irAE dermatitis, as well as IFNγ within TRM cells specifically. The Th1-skewed phenotype was confirmed in irAE colitis cases compared with healthy colon.
MeSH term(s)	CTLA-4 Antigen ; Colitis/chemically induced ; Cytokines/metabolism ; Dermatitis ; Humans ; Immune Checkpoint Inhibitors ; Memory T Cells ; Programmed Cell Death 1 Receptor ; Psoriasis ; RNA ; Tumor Necrosis Factor-alpha
Chemical Substances	CTLA-4 Antigen ; Cytokines ; Immune Checkpoint Inhibitors ; Programmed Cell Death 1 Receptor ; Tumor Necrosis Factor-alpha ; RNA (63231-63-0)
Language	English
Publishing date	2022-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-22-0362
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Zs.A 7022: Show issues

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Article ; Online: Insights from a Rapidly Implemented COVID-19 Biobank Using Electronic Consent and Informatics Tools.

Higgs, Emily F / Flood, Blake A / Pyzer, Athalia R / Rouhani, Sherin J / Trujillo, Jonathan A / Gajewski, Thomas F

Biopreservation and biobanking

2022 Volume 21, Issue 2, Page(s) 166–175

Abstract: Biobanking during the COVID-19 pandemic presented unique challenges regarding patient enrollment, sample collection, and experimental analysis. This report details the ways in which we rapidly overcame those challenges to create a robust database of ... ...

Abstract	Biobanking during the COVID-19 pandemic presented unique challenges regarding patient enrollment, sample collection, and experimental analysis. This report details the ways in which we rapidly overcame those challenges to create a robust database of clinical information and patient samples while maintaining clinician and researcher safety. We developed a pipeline using REDCap (Research Electronic Data Capture) to coordinate electronic informed consent, sample collection, immunological assay execution, and data analysis for biobanking samples from patients with COVID-19. We then integrated immunological assay data with clinical data extracted from the electronic health record to link study parameters with clinical readouts. Of the 193 inpatients who participated in this study, 138 consented electronically and 56 provided paper consent. We collected and banked blood samples to measure circulating cytokines and chemokines, peripheral immune cell composition and activation status, anti-COVID-19 antibodies, and germline gene polymorphisms. In addition, we collected DNA and RNA from nasopharyngeal swabs to assess viral titer and microbiome composition by 16S sequencing. The rapid spread and contagious nature of COVID-19 required special considerations and innovative solutions to biobank samples quickly while protecting researchers and clinicians. Overall, this workflow and computational pipeline allowed for comprehensive immune profiling of 193 inpatients infected with COVID-19, as well as 89 outpatients, 157 patients receiving curbside COVID-19 testing, and 86 healthy controls. We describe a novel electronic framework for biobanking and analyzing patient samples during COVID-19, and present insights and strategies that can be applied more broadly to other biobank studies.
MeSH term(s)	Humans ; COVID-19/epidemiology ; Biological Specimen Banks ; COVID-19 Testing ; Pandemics ; Informed Consent ; Databases, Factual
Language	English
Publishing date	2022-06-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2593993-2
ISSN	1947-5543 ; 1947-5535
ISSN (online)	1947-5543
ISSN	1947-5535
DOI	10.1089/bio.2021.0169
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Article ; Online: Lymphatic coagulation and neutrophil extracellular traps in lung-draining lymph nodes of COVID-19 decedents.

Blood advances

2024 Volume 6, Issue 24, Page(s) 6249–6262

Abstract: Clinical manifestations of severe COVID-19 include coagulopathies that are exacerbated by the formation of neutrophil extracellular traps (NETs). Here, we report that pulmonary lymphatic vessels, which traffic neutrophils and other immune cells to the ... ...

Abstract	Clinical manifestations of severe COVID-19 include coagulopathies that are exacerbated by the formation of neutrophil extracellular traps (NETs). Here, we report that pulmonary lymphatic vessels, which traffic neutrophils and other immune cells to the lung-draining lymph node (LDLN), can also be blocked by fibrin clots in severe COVID-19. Immunostained tissue sections from COVID-19 decedents revealed widespread lymphatic clotting not only in the lung but also in the LDLN, where the extent of clotting correlated with the presence of abnormal, regressed, or missing germinal centers (GCs). It strongly correlated with the presence of intralymphatic NETs. In mice, tumor necrosis factor α induced intralymphatic fibrin clots; this could be inhibited by DNase I, which degrades NETs. In vitro, TNF-α induced lymphatic endothelial cell upregulation of ICAM-1 and CXCL8, among other neutrophil-recruiting factors, as well as thrombomodulin downregulation; in decedents, lymphatic clotting in LDLNs. In a separate cohort of hospitalized patients, serum levels of Myeloperoxidase-DNA (MPO-DNA, a NET marker) inversely correlated with antiviral antibody titers, but D-dimer levels, indicative of blood thrombosis, did not correlate with either. Patients with high MPO-DNA but low D-dimer levels generated poor antiviral antibody titers. This study introduces lymphatic coagulation in lungs and LDLNs as a clinical manifestation of severe COVID-19 and suggests the involvement of NETosis of lymphatic-trafficking neutrophils. It further suggests that lymphatic clotting may correlate with impaired formation or maintenance of GCs necessary for robust antiviral antibody responses, although further studies are needed to determine whether and how lymphatic coagulation affects adaptive immune responses.
MeSH term(s)	Mice ; Animals ; Extracellular Traps ; COVID-19 ; Thrombosis/metabolism ; Lung/metabolism ; DNA/metabolism ; Lymph Nodes
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2022007798
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Article ; Online: Severe COVID-19 induces autoantibodies against angiotensin II that correlate with blood pressure dysregulation and disease severity.

Briquez, Priscilla S / Rouhani, Sherin J / Yu, Jovian / Pyzer, Athalia R / Trujillo, Jonathan / Dugan, Haley L / Stamper, Christopher T / Changrob, Siriruk / Sperling, Anne I / Wilson, Patrick C / Gajewski, Thomas F / Hubbell, Jeffrey A / Swartz, Melody A

Science advances

2022 Volume 8, Issue 40, Page(s) eabn3777

Abstract: Patients infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can experience life-threatening respiratory distress, blood pressure dysregulation, and thrombosis. This is thought to be associated with an impaired activity of ... ...

Abstract	Patients infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can experience life-threatening respiratory distress, blood pressure dysregulation, and thrombosis. This is thought to be associated with an impaired activity of angiotensin-converting enzyme 2 (ACE2), which is the main entry receptor of SARS-CoV-2 and which also tightly regulates blood pressure by converting the vasoconstrictive peptide angiotensin II (AngII) to a vasopressor peptide. Here, we show that a significant proportion of hospitalized patients with COVID-19 developed autoantibodies against AngII, whose presence correlates with lower blood oxygenation, blood pressure dysregulation, and overall higher disease severity. Anti-AngII antibodies can develop upon specific immune reaction to the SARS-CoV-2 proteins Spike or receptor-binding domain (RBD), to which they can cross-bind, suggesting some epitope mimicry between AngII and Spike/RBD. These results provide important insights on how an immune reaction against SARS-CoV-2 can impair blood pressure regulation.
MeSH term(s)	Angiotensin II ; Angiotensin-Converting Enzyme 2 ; Autoantibodies ; Blood Pressure ; COVID-19 ; Epitopes/metabolism ; Humans ; Peptidyl-Dipeptidase A/metabolism ; Protein Binding ; SARS-CoV-2 ; Severity of Illness Index ; Spike Glycoprotein, Coronavirus
Chemical Substances	Autoantibodies ; Epitopes ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; Angiotensin II (11128-99-7) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2022-10-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abn3777
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Article ; Online: STK11

JCO precision oncology

2023 Volume 7, Page(s) e2200273

Abstract: Purpose: Molecular factors predicting relapse in early-stage non-small-cell lung cancer (ES-NSCLC) are poorly understood, especially in inoperable patients receiving radiotherapy (RT). In this study, we compared the genomic profiles of inoperable and ... ...

Abstract	Purpose: Molecular factors predicting relapse in early-stage non-small-cell lung cancer (ES-NSCLC) are poorly understood, especially in inoperable patients receiving radiotherapy (RT). In this study, we compared the genomic profiles of inoperable and operable ES-NSCLC. Materials and methods: This retrospective study included 53 patients with nonsquamous ES-NSCLC (stage I-II) treated at a single institution (University of Chicago) with surgery (ie, operable; n = 30) or RT (ie, inoperable; n = 23) who underwent tumor genomic profiling. A second cohort of ES-NSCLC treated with RT (Stanford, n = 39) was included to power clinical analyses. Prognostic gene alterations were identified and correlated with clinical variables. The primary clinical end point was the correlation of prognostic genes with the cumulative incidence of relapse, disease-free survival, and overall survival (OS) in a pooled RT cohort from the two institutions (N = 62). Results: Although the surgery cohort exhibited lower rates of relapse, the RT cohort was highly enriched for somatic Conclusion: In this cohort of ES-NSCLC,
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/therapy ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Lung Neoplasms/drug therapy ; Retrospective Studies ; Neoplasm Staging ; Neoplasm Recurrence, Local/epidemiology ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/pathology ; Small Cell Lung Carcinoma ; AMP-Activated Protein Kinase Kinases
Chemical Substances	STK11 protein, human (EC 2.7.11.1) ; AMP-Activated Protein Kinase Kinases (EC 2.7.11.3)
Language	English
Publishing date	2023-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2473-4284
ISSN (online)	2473-4284
DOI	10.1200/PO.22.00273
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Article: SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II.

medRxiv : the preprint server for health sciences

2021

Abstract: Patients infected with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can experience life-threatening respiratory distress, blood pressure dysregulation and thrombosis. This is thought to be associated with an impaired activity of ... ...

Abstract	Patients infected with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can experience life-threatening respiratory distress, blood pressure dysregulation and thrombosis. This is thought to be associated with an impaired activity of angiotensin-converting enzyme-2 (ACE-2), which is the main entry receptor of SARS-CoV-2 and which also tightly regulates blood pressure by converting the vasoconstrictive peptide angiotensin II (AngII) to a vasopressor peptide. Here, we show that a significant proportion of hospitalized COVID-19 patients developed autoantibodies against AngII, whose presence correlates with lower blood oxygenation, blood pressure dysregulation, and overall higher disease severity. Anti-AngII antibodies can develop upon specific immune reaction to the SARS-CoV-2 proteins Spike or RBD, to which they can cross-bind, suggesting some epitope mimicry between AngII and Spike/RBD. These results provide important insights on how an immune reaction against SARS-CoV-2 can impair blood pressure regulation.
Language	English
Publishing date	2021-11-02
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.11.02.21265789
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