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Article ; Online: Pancreatic Cancer Thrives on Hijacking a Homeostatic Tissue Repair Pathway.

Pylayeva-Gupta, Yuliya

2020 Volume 158, Issue 5, Page(s) 1216–1218

MeSH term(s)	Acinar Cells ; Animals ; Cell Plasticity ; Interleukins ; Mice ; Pancreatic Neoplasms
Chemical Substances	Interleukins
Language	English
Publishing date	2020-02-10
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2020.02.010
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Article: IL-12 Family Cytokines in Cancer and Immunotherapy.

Mirlekar, Bhalchandra / Pylayeva-Gupta, Yuliya

Cancers

2021 Volume 13, Issue 2

Abstract: The IL-12 family cytokines are a group of unique heterodimeric cytokines that include IL-12, IL-23, IL-27, IL-35 and, most recently, IL-39. Recent studies have solidified the importance of IL-12 cytokines in shaping innate and adaptive immune responses ... ...

Abstract	The IL-12 family cytokines are a group of unique heterodimeric cytokines that include IL-12, IL-23, IL-27, IL-35 and, most recently, IL-39. Recent studies have solidified the importance of IL-12 cytokines in shaping innate and adaptive immune responses in cancer and identified multipronged roles for distinct IL-12 family members, ranging from effector to regulatory immune functions. These cytokines could serve as promising candidates for the development of immunomodulatory therapeutic approaches. Overall, IL-12 can be considered an effector cytokine and has been found to engage anti-tumor immunity by activating the effector Th1 response, which is required for the activation of cytotoxic T and NK cells and tumor clearance. IL-23 and IL-27 play dual roles in tumor immunity, as they can both activate effector immune responses and promote tumor growth by favoring immune suppression. IL-35 is a potent regulatory cytokine and plays a largely pro-tumorigenic role by inhibiting effector T cells. In this review, we summarize the recent findings on IL-12 family cytokines in the control of tumor growth with an emphasis primarily on immune regulation. We underscore the clinical implications for the use of these cytokines either in the setting of monotherapy or in combination with other conventional therapies for the more effective treatment of malignancies.
Language	English
Publishing date	2021-01-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13020167
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Article ; Online: IL-35 Detection in B Cells at the mRNA and Protein Level.

Mirlekar, Bhalchandra / Michaud, Daniel / Pylayeva-Gupta, Yuliya

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2270, Page(s) 125–147

Abstract: Emerging research suggests that IL-35-producing regulatory B cells accumulate in patients and mouse models of pancreatic cancer, one of the most lethal cancers, characterized by late diagnosis, high mortality, and morbidity. Identification of IL-35- ... ...

Abstract	Emerging research suggests that IL-35-producing regulatory B cells accumulate in patients and mouse models of pancreatic cancer, one of the most lethal cancers, characterized by late diagnosis, high mortality, and morbidity. Identification of IL-35-producing B cells can be challenging due to the heterodimeric nature of IL-35 and diversity of cell surface markers that define regulatory B-cell subsets across spectrum of diseases. In this chapter, we describe the methods for the isolation of splenic and tumor-infiltrating murine regulatory B cells and subsequent detection of IL-35 by RT-qPCR and intracellular staining, as well as detection of circulating IL-35 by ELISA. We also describe methods for the detection of IL-35-producing human B cells by flow cytometry, RT-qPCR, and immunofluorescence in the context of pancreatic cancer. This chapter should facilitate the study of regulatory IL-35
MeSH term(s)	Animals ; B-Lymphocyte Subsets/cytology ; B-Lymphocyte Subsets/immunology ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; B-Lymphocytes, Regulatory/immunology ; Cytokines/metabolism ; Enzyme-Linked Immunosorbent Assay/methods ; Flow Cytometry/methods ; Humans ; Interleukin-10/immunology ; Interleukins/analysis ; Interleukins/blood ; Mice ; RNA, Messenger/analysis ; RNA, Messenger/genetics ; Reverse Transcriptase Polymerase Chain Reaction/methods
Chemical Substances	Cytokines ; Interleukins ; RNA, Messenger ; interleukin-35, human ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2021-01-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1237-8_8
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Article: Molecular Pathways: Interleukin-35 in Autoimmunity and Cancer.

Pylayeva-Gupta, Yuliya

Clinical cancer research : an official journal of the American Association for Cancer Research

2016 Volume 22, Issue 20, Page(s) 4973–4978

Abstract: Immunosuppressive functions conferred by regulatory cytokines are important for maintaining homeostasis in immune responses. IL35 has recently emerged as a novel regulator of immune responses. Once thought to be specifically expressed by T regulatory ... ...

Abstract	Immunosuppressive functions conferred by regulatory cytokines are important for maintaining homeostasis in immune responses. IL35 has recently emerged as a novel regulator of immune responses. Once thought to be specifically expressed by T regulatory cells, induction of IL35 expression has now been detected in multiple cell types in a variety of diseases, prompting research into regulation of its expression, signaling specificity, target cell populations, and functional outputs. Recent studies have revealed that by directing de novo generation of regulatory T and B cells and inhibiting T effector responses, IL35 plays an important role in the development of autoimmune diseases and cancer. IL35 is overexpressed in a variety of cancers and may exert its function both on antitumor immune responses as well as directly on tumor cells. As such, IL35 is rapidly emerging as a promising biomarker and an attractive cancer therapy target. Clin Cancer Res; 22(20); 4973-8. ©2016 AACR.
Language	English
Publishing date	2016-10-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-16-0743
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Article ; Online: Focused Ultrasound for Immunomodulation of the Tumor Microenvironment.

Joiner, Jordan B / Pylayeva-Gupta, Yuliya / Dayton, Paul A

Journal of immunology (Baltimore, Md. : 1950)

2020 Volume 205, Issue 9, Page(s) 2327–2341

Abstract: Focused ultrasound (FUS) has recently emerged as a modulator of the tumor microenvironment, paving the way for FUS to become a safe yet formidable cancer treatment option. Several mechanisms have been proposed for the role of FUS in facilitating immune ... ...

Abstract	Focused ultrasound (FUS) has recently emerged as a modulator of the tumor microenvironment, paving the way for FUS to become a safe yet formidable cancer treatment option. Several mechanisms have been proposed for the role of FUS in facilitating immune responses and overcoming drug delivery barriers. However, with the wide variety of FUS parameters used in diverse tumor types, it is challenging to pinpoint FUS specifications that may elicit the desired antitumor response. To clarify FUS bioeffects, we summarize four mechanisms of action, including thermal ablation, hyperthermia/thermal stress, mechanical perturbation, and histotripsy, each inducing unique vascular and immunological effects. Notable tumor responses to FUS include enhanced vascular permeability, increased T cell infiltration, and tumor growth suppression. In this review, we have categorized and reviewed recent methods of using therapeutic ultrasound to elicit an antitumor immune response with examples that reveal specific solutions and challenges in this new research area.
MeSH term(s)	Animals ; Drug Delivery Systems/methods ; Humans ; Immunity/immunology ; Immunomodulation/immunology ; Neoplasms/immunology ; Neoplasms/therapy ; Tumor Microenvironment/immunology ; Ultrasonic Therapy/methods
Language	English
Publishing date	2020-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1901430
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Article ; Online: B Cell Receptor Signaling and Protein Kinase D2 Support Regulatory B Cell Function in Pancreatic Cancer.

Michaud, Daniel / Mirlekar, Bhalchandra / Steward, Colleen / Bishop, Gail / Pylayeva-Gupta, Yuliya

Frontiers in immunology

2022 Volume 12, Page(s) 745873

Abstract: B cells can act as potent suppressors of anti-tumor T cell immunity, presenting a mechanism of resistance to immunotherapy. In pancreatic ductal adenocarcinoma, B cells can display a T cell-suppressive or regulatory phenotype centered on the expression ... ...

Abstract	B cells can act as potent suppressors of anti-tumor T cell immunity, presenting a mechanism of resistance to immunotherapy. In pancreatic ductal adenocarcinoma, B cells can display a T cell-suppressive or regulatory phenotype centered on the expression of the cytokine Interleukin 35 (IL-35). While B cell-mediated immunosuppression presents a barrier to anti-tumorigenic T cell function, it is not clear how regulatory B cell function could be targeted, and the signals that promote this suppressive phenotype in B cells are not well understood. Here we use a novel IL-35 reporter model to understand which signaling pathways are important for immunosuppressive properties in B cells.
MeSH term(s)	Animals ; B-Lymphocytes, Regulatory/immunology ; Carcinoma, Pancreatic Ductal/immunology ; Interleukins/biosynthesis ; Interleukins/immunology ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms/immunology ; Protein Kinase D2/immunology ; Receptors, Antigen, B-Cell/immunology ; Signal Transduction/immunology
Chemical Substances	Interleukins ; Protein Kinase D2 ; Receptors, Antigen, B-Cell ; interleukin-35, mouse
Language	English
Publishing date	2022-01-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.745873
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Article ; Online: Regulatory B cells in cancer.

Michaud, Daniel / Steward, Colleen R / Mirlekar, Bhalchandra / Pylayeva-Gupta, Yuliya

Immunological reviews

2020 Volume 299, Issue 1, Page(s) 74–92

Abstract: Tumorigenesis proceeds through discrete steps where acquisition of genetic lesions and changes in the surrounding microenvironment combine to drive unrestricted neoplastic proliferation and metastasis. The ability of tumor-infiltrating immune cells to ... ...

Abstract	Tumorigenesis proceeds through discrete steps where acquisition of genetic lesions and changes in the surrounding microenvironment combine to drive unrestricted neoplastic proliferation and metastasis. The ability of tumor-infiltrating immune cells to promote tumor growth via the provision of signals that enable tumor cell survival and proliferation as well as contribute to immune suppression is an active area of research. Recent efforts have provided us with mechanistic insights into how B cells can positively and negatively regulate immune responses. Negative regulation of immune responses in cancer can be mediated by regulatory B cells and is often a result of increased production of cytokines that can directly and indirectly affect anti-tumor immune function and cancer cell growth. Signals that lead to the expansion of regulatory B cells and the spectrum of their functional roles are not well understood and are the subject of active research by many groups. Here, we elaborate broadly on the history of regulatory B cells in cancer and summarize recent studies that have established genetic models for the study of regulatory B cell function and their potential for therapeutic intervention in the setting of solid cancers.
MeSH term(s)	B-Lymphocytes, Regulatory ; Cytokines ; Humans ; Immunity ; Neoplasms ; Tumor Microenvironment
Chemical Substances	Cytokines
Language	English
Publishing date	2020-12-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.12939
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Article ; Online: Low-Intensity Focused Ultrasound Produces Immune Response in Pancreatic Cancer.

Joiner, Jordan B / Kren, Nancy P / Durham, Phillip G / McRee, Autumn J / Dayton, Paul A / Pylayeva-Gupta, Yuliya

Ultrasound in medicine & biology

2022 Volume 48, Issue 11, Page(s) 2344–2353

Abstract: Pancreatic adenocarcinoma is an aggressive malignancy with limited therapeutic treatments available and a 5-y survival less than 10%. Pancreatic cancers have been found to be immunogenically "cold" with a largely immunosuppressive tumor microenvironment. ...

Abstract	Pancreatic adenocarcinoma is an aggressive malignancy with limited therapeutic treatments available and a 5-y survival less than 10%. Pancreatic cancers have been found to be immunogenically "cold" with a largely immunosuppressive tumor microenvironment. There is emerging evidence that focused ultrasound can induce changes in the tumor microenvironment and have a constructive impact on the effect of immunotherapy. However, the immune cells and timing involved in these effects remain unclear, which is essential to determining how to combine immunotherapy with ultrasound for treatment of pancreatic adenocarcinoma. We used low-intensity focused ultrasound and microbubbles (LoFU + MBs), which can mechanically disrupt cellular membranes and vascular endothelia, to treat subcutaneous pancreatic tumors in C57BL/6 mice. To evaluate the immune cell landscape and expression and/or localization of damage-associated molecular patterns (DAMPs) as a response to ultrasound, we performed flow cytometry and histology on tumors and draining lymph nodes 2 and 15 d post-treatment. We repeated this study on larger tumors and with multiple treatments to determine whether similar or greater effects could be achieved. Two days after treatment, draining lymph nodes exhibited a significant increase in activated antigen presenting cells, such as macrophages, as well as expansion of CD8
MeSH term(s)	Adenocarcinoma/immunology ; Adenocarcinoma/therapy ; Animals ; CD8-Positive T-Lymphocytes/immunology ; HMGB1 Protein ; Immunity ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/therapy ; Tumor Microenvironment ; Ultrasonic Therapy
Chemical Substances	HMGB1 Protein
Language	English
Publishing date	2022-08-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	186150-5
ISSN	1879-291X ; 0301-5629
ISSN (online)	1879-291X
ISSN	0301-5629
DOI	10.1016/j.ultrasmedbio.2022.06.017
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Article ; Online: Rab27a plays a dual role in metastatic propensity of pancreatic cancer.

Kren, Nancy / Michaud, Daniel / Bagchi, Sukriti / Greene, Kevin / Pylayeva-Gupta, Yuliya

Scientific reports

2020 Volume 10, Issue 1, Page(s) 7390

Abstract: Pancreatic cancer is an aggressive malignancy, often diagnosed at metastatic stages. Several studies have implicated systemic factors, such as extracellular vesicle release and myeloid cell expansion, in the establishment of pre-metastatic niches in ... ...

Abstract	Pancreatic cancer is an aggressive malignancy, often diagnosed at metastatic stages. Several studies have implicated systemic factors, such as extracellular vesicle release and myeloid cell expansion, in the establishment of pre-metastatic niches in cancer. The Rab27a GTPase is overexpressed in advanced cancers, can regulate vesicle trafficking, and has been previously linked to non-cell autonomous control of tumor growth and metastasis, however, the role of Rab27a itself in the metastatic propensity of pancreatic cancer is not well understood. Here, we have established a model to study how Rab27a directs formation of the pre-metastatic niche. Loss of Rab27a in pancreatic cancer cells did not decrease tumor growth in vivo, but resulted in altered systemic myeloid cell expansion, both in the primary tumors and at the distant organ sites. In metastasis assays, loss of Rab27a expression in tumor cells injected into circulation compromised efficient outgrowth of metastatic lesions. However, Rab27a knockdown cells had an unexpected advantage at initial steps of metastatic seeding, suggesting that Rab27a may alter cell-autonomous invasive properties of the tumor cells. Gene expression analysis of gene expression revealed that downregulation of Rab27a increased expression of genes involved in epithelial-to-mesenchymal transition pathways, consistent with our findings that primary tumors arising from Rab27a knockdown cells were more invasive. Overall, these data reveal that Rab27a can play divergent roles in regulating pro-metastatic propensity of pancreatic cancer cells: by generating pro-metastatic environment at the distant organ sites, and by suppressing invasive properties of the cancer cells.
MeSH term(s)	Animals ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Male ; Mice ; Neoplasm Metastasis ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Pancreatic Neoplasms/enzymology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; rab27 GTP-Binding Proteins/biosynthesis ; rab27 GTP-Binding Proteins/genetics
Chemical Substances	Neoplasm Proteins ; rab27 GTP-Binding Proteins ; Rab27a protein, mouse (EC 3.6.1.-.)
Language	English
Publishing date	2020-04-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-64248-1
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Article ; Online: Gut epithelial Interleukin-17 receptor A signaling can modulate distant tumors growth through microbial regulation.

Chandra, Vidhi / Li, Le / Le Roux, Olivereen / Zhang, Yu / Howell, Rian M / Rupani, Dhwani N / Baydogan, Seyda / Miller, Haiyan D / Riquelme, Erick / Petrosino, Joseph / Kim, Michael P / Bhat, Krishna P L / White, James R / Kolls, Jay K / Pylayeva-Gupta, Yuliya / McAllister, Florencia

Cancer cell

2023 Volume 42, Issue 1, Page(s) 85–100.e6

Abstract: Microbes influence cancer initiation, progression and therapy responsiveness. IL-17 signaling contributes to gut barrier immunity by regulating microbes but also drives tumor growth. A knowledge gap remains regarding the influence of enteric IL-17-IL- ... ...

Abstract	Microbes influence cancer initiation, progression and therapy responsiveness. IL-17 signaling contributes to gut barrier immunity by regulating microbes but also drives tumor growth. A knowledge gap remains regarding the influence of enteric IL-17-IL-17RA signaling and their microbial regulation on the behavior of distant tumors. We demonstrate that gut dysbiosis induced by systemic or gut epithelial deletion of IL-17RA induces growth of pancreatic and brain tumors due to excessive development of Th17, primary source of IL-17 in human and mouse pancreatic ductal adenocarcinoma, as well as B cells that circulate to distant tumors. Microbial dependent IL-17 signaling increases DUOX2 signaling in tumor cells. Inefficacy of pharmacological inhibition of IL-17RA is overcome with targeted microbial ablation that blocks the compensatory loop. These findings demonstrate the complexities of IL-17-IL-17RA signaling in different compartments and the relevance for accounting for its homeostatic host defense function during cancer therapy.
MeSH term(s)	Mice ; Animals ; Humans ; Interleukin-17 ; Receptors, Interleukin-17/genetics ; Mice, Knockout ; Signal Transduction ; Pancreatic Neoplasms/pathology
Chemical Substances	Interleukin-17 ; Receptors, Interleukin-17
Language	English
Publishing date	2023-12-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2023.12.006
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