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  1. Article: Interleukin-18 Binding Protein (IL-18BP): A Long Journey From Discovery to Clinical Application.

    Kim, Soohyun / Yu, Hyeon / Azam, Tania / Dinarello, Charles A

    Immune network

    2024  Volume 24, Issue 1, Page(s) e1

    Abstract: IL-18 binding protein (IL-18BP) was originally discovered in 1999 while attempting to identify an IL-18 receptor ligand binding chain (also known as IL-18Rα) by subjecting concentrated human urine to an IL-18 ligand affinity column. The IL-18 ligand ... ...

    Abstract IL-18 binding protein (IL-18BP) was originally discovered in 1999 while attempting to identify an IL-18 receptor ligand binding chain (also known as IL-18Rα) by subjecting concentrated human urine to an IL-18 ligand affinity column. The IL-18 ligand chromatography purified molecule was analyzed by protein microsequencing. The result revealed a novel 40 amino acid polypeptide. To isolate the complete open reading frame (ORF), various human and mouse cDNA libraries were screened using cDNA probe derived from the novel IL-18 affinity column bound molecule. The identified entire ORF gene was thought to be an IL-18Rα gene. However, IL-18BP has been proven to be a unique soluble antagonist that shares homology with a variety of viral proteins that are distinct from the IL-18Rα and IL-18Rβ chains. The IL-18BP cDNA was used to generate recombinant IL-18BP (rIL-18BP), which was indispensable for characterizing the role of IL-18BP
    Language English
    Publishing date 2024-01-15
    Publishing country Korea (South)
    Document type Journal Article ; Review
    ZDB-ID 2536191-0
    ISSN 2092-6685 ; 1598-2629
    ISSN (online) 2092-6685
    ISSN 1598-2629
    DOI 10.4110/in.2024.24.e1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Perspective: Daniela Novick, cytokines and their receptors.

    Ghezzi, Pietro / Fantuzzi, Giamila / Dinarello, Charles A

    Frontiers in immunology

    2023  Volume 14, Page(s) 1160651

    Abstract: This Perspective highlights the work of Dr. Daniela Novick in the field of cytokine biology. Using affinity chromatography to characterize cytokine-binding proteins, she identified soluble forms of the receptors as well as binding proteins for several ... ...

    Abstract This Perspective highlights the work of Dr. Daniela Novick in the field of cytokine biology. Using affinity chromatography to characterize cytokine-binding proteins, she identified soluble forms of the receptors as well as binding proteins for several cytokines, including tumor necrosis factor, interleukin (IL) 6, IL-18 and IL-32. Importantly, her work has been key in the development of monoclonal antibodies against interferons and cytokines. This Perspective discusses her contribution to the field and highlights her recent review on this topic.
    MeSH term(s) Female ; Humans ; Cytokines/metabolism ; Interleukin-6/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Interferons ; Antibodies, Monoclonal/therapeutic use
    Chemical Substances Cytokines ; Interleukin-6 ; Tumor Necrosis Factor-alpha ; Interferons (9008-11-1) ; Antibodies, Monoclonal
    Language English
    Publishing date 2023-05-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1160651
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  3. Article ; Online: NLRP3 and cancer: Pathogenesis and therapeutic opportunities.

    Tengesdal, Isak W / Dinarello, Charles A / Marchetti, Carlo

    Pharmacology & therapeutics

    2023  Volume 251, Page(s) 108545

    Abstract: More than a decade ago IL-1 blockade was suggested as an add-on therapy for the treatment of cancer. This proposal was based on the overall safety record of anti-IL-1 biologics and the anti-tumor properties of IL-1 blockade in animal models of cancer. ... ...

    Abstract More than a decade ago IL-1 blockade was suggested as an add-on therapy for the treatment of cancer. This proposal was based on the overall safety record of anti-IL-1 biologics and the anti-tumor properties of IL-1 blockade in animal models of cancer. Today, a new frontier in IL-1 activity regulation has developed with several orally active NLRP3 inhibitors currently in clinical trials, including cancer. Despite an increasing body of evidence suggesting a role of NLRP3 and IL-1-mediated inflammation driving cancer initiation, immunosuppression, growth, and metastasis, NLRP3 activation in cancer remains controversial. In this review, we discuss the recent advances in the understanding of NLRP3 activation in cancer. Further, we discuss the current opportunities for NLRP3 inhibition in cancer intervention with novel small molecules.
    MeSH term(s) Animals ; Inflammasomes ; Inflammation/drug therapy ; Interleukin-1 ; Neoplasms/drug therapy ; NLR Family, Pyrin Domain-Containing 3 Protein/physiology ; Reactive Oxygen Species
    Chemical Substances Inflammasomes ; Interleukin-1 ; NLR Family, Pyrin Domain-Containing 3 Protein ; Reactive Oxygen Species ; NLRP3 protein, human
    Language English
    Publishing date 2023-10-21
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 194735-7
    ISSN 1879-016X ; 0163-7258
    ISSN (online) 1879-016X
    ISSN 0163-7258
    DOI 10.1016/j.pharmthera.2023.108545
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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: Dexamethasone and OLT1177 Cooperate in the Reduction of Melanoma Growth by Inhibiting STAT3 Functions.

    Dinarello, Alberto / Mills, Taylor S / Tengesdal, Isak W / Powers, Nicholas E / Azam, Tania / Dinarello, Charles A

    Cells

    2023  Volume 12, Issue 2

    Abstract: The NLRP3 inflammasome is a multimolecular complex that processes inactive IL-1β and IL-18 into proinflammatory cytokines. OLT1177 is an orally active small compound that specifically inhibits NLRP3. Here, B16F10 melanoma were implanted in mice and ... ...

    Abstract The NLRP3 inflammasome is a multimolecular complex that processes inactive IL-1β and IL-18 into proinflammatory cytokines. OLT1177 is an orally active small compound that specifically inhibits NLRP3. Here, B16F10 melanoma were implanted in mice and treated with OLT1177 as well as combined with the glucocorticoid dexamethasone. At sacrifice, OLT1177 treated mice had significantly smaller tumors compared to tumor-bearing mice treated with vehicle. However, the combined treatment of OLT1177 plus dexamethasone revealed a greater suppression of tumor growth. This reduction was accompanied by a downregulation of nuclear and mitochondrial STAT3-dependent gene transcription and by a significant reduction of STAT3 Y705 and S727 phosphorylations in the tumors. In vitro, the human melanoma cell line 1205Lu, stimulated with IL-1α, exhibited significantly lower levels of STAT3 Y705 phosphorylation by the combination treatment, thus affecting the nuclear functions of STAT3. In the same cells, STAT3 serine 727 phosphorylation was also lower, affecting the mitochondrial functions of STAT3. In addition, metabolic analyses revealed a marked reduction of ATP production rate and glycolytic reserve in cells treated with the combination of OLT1177 plus dexamethasone. These findings demonstrate that the combination of OLT1177 and dexamethasone reduces tumor growth by targeting nuclear as well as mitochondrial functions of STAT3.
    MeSH term(s) Humans ; Animals ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Inflammasomes/metabolism ; Melanoma/drug therapy ; Dexamethasone/pharmacology ; Dexamethasone/therapeutic use ; STAT3 Transcription Factor/metabolism
    Chemical Substances NLR Family, Pyrin Domain-Containing 3 Protein ; dapansutrile (2Z03364G96) ; Inflammasomes ; Dexamethasone (7S5I7G3JQL) ; STAT3 protein, human ; STAT3 Transcription Factor
    Language English
    Publishing date 2023-01-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12020294
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  5. Article: Treatment of Inflammatory Diseases with IL-1 Blockade.

    Dinarello, Charles A

    Current otorhinolaryngology reports

    2018  Volume 6, Issue 1, Page(s) 1–14

    Abstract: Background: Autoinflammatory diseases are distinct from autoimmune diseases. Whereas autoinflammatory diseases are due to dysfunctional T-cells and B-cells, autoinflammatory diseases are due to overproduction of macrophage cytokines particularly ... ...

    Abstract Background: Autoinflammatory diseases are distinct from autoimmune diseases. Whereas autoinflammatory diseases are due to dysfunctional T-cells and B-cells, autoinflammatory diseases are due to overproduction of macrophage cytokines particularly interleukin-1 beta (IL-1β). A causative role for IL-1 in autoinflammatory diseases is derived from clinical studies blocking the IL-1 receptor or neutralizing monoclonal antibodies or soluble receptors.
    Methods: A review was performed of clinical trials in autoinflammatory diseases using the IL-1 receptor antagonist (anakinra), the soluble IL-1 receptor (rilonacept), antibodies to IL-1β (canakinumab, gevokizumab) and anti-IL-1α (xilonix).
    Findings: Anakinra blocks the IL-1 Receptor type 1 (IL-1R1) and therefore blocks the activities of both IL-1α and IL-1β. Off-label use of anakinra is common for a broad spectrum of inflammatory diseases. Neutralization of IL-1β is used to treat hereditary autoinflammatory diseases but also atherosclerosis. Rilonacept reduces arterial wall inflammation in patients with chronic kidney disease. Neutralization of IL-1α has prolonged life in patients with advanced metastatic colorectal cancer. Compared to other cytokine blocking therapies, reducing the activities of IL-1 has an excellent safety record.
    Conclusions: Blocking IL-1 therapies can be used to treat a wide-spectrum of acute and chronic inflammatory diseases.
    Language English
    Publishing date 2018-03-07
    Publishing country Switzerland
    Document type Journal Article
    ISSN 2167-583X
    ISSN 2167-583X
    DOI 10.1007/s40136-018-0181-9
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  6. Article ; Online: Pharmacologic inhibition of NLRP3 reduces the levels of α-synuclein and protects dopaminergic neurons in a model of Parkinson's disease.

    Amo-Aparicio, Jesus / Daly, Jonathan / Højen, Jesper Falkesgaard / Dinarello, Charles A

    Journal of neuroinflammation

    2023  Volume 20, Issue 1, Page(s) 147

    Abstract: Background: Parkinson's disease (PD) is characterized by a progressive degeneration of dopaminergic neurons, which leads to irreversible loss of peripheral motor functions. Death of dopaminergic neurons induces an inflammatory response in microglial ... ...

    Abstract Background: Parkinson's disease (PD) is characterized by a progressive degeneration of dopaminergic neurons, which leads to irreversible loss of peripheral motor functions. Death of dopaminergic neurons induces an inflammatory response in microglial cells, which further exacerbates neuronal loss. Reducing inflammation is expected to ameliorate neuronal loss and arrest motor dysfunctions. Because of the contribution of the NLRP3 inflammasome to the inflammatory response in PD, we targeted NLRP3 using the specific inhibitor OLT1177
    Methods: We evaluated the effectiveness of OLT1177
    Results: Treatment with OLT1177
    Conclusions: These data suggest that targeting the NLRP3 inflammasome by OLT1177
    MeSH term(s) Humans ; Animals ; Mice ; Parkinson Disease/drug therapy ; alpha-Synuclein/pharmacology ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Dopaminergic Neurons ; Mice, Inbred C57BL ; Disease Models, Animal
    Chemical Substances alpha-Synuclein ; Inflammasomes ; dapansutrile (2Z03364G96) ; NLR Family, Pyrin Domain-Containing 3 Protein
    Language English
    Publishing date 2023-06-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-023-02830-w
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  7. Article: Metabolic reprogramming of the inflammatory response in the nervous system: the crossover between inflammation and metabolism.

    Amo-Aparicio, Jesus / Dinarello, Charles A / Lopez-Vales, Ruben

    Neural regeneration research

    2023  Volume 19, Issue 10, Page(s) 2189–2201

    Abstract: Metabolism is a fundamental process by which biochemicals are broken down to produce energy (catabolism) or used to build macromolecules (anabolism). Metabolism has received renewed attention as a mechanism that generates molecules that modulate multiple ...

    Abstract Metabolism is a fundamental process by which biochemicals are broken down to produce energy (catabolism) or used to build macromolecules (anabolism). Metabolism has received renewed attention as a mechanism that generates molecules that modulate multiple cellular responses. This was first identified in cancer cells as the Warburg effect, but it is also present in immunocompetent cells. Studies have revealed a bidirectional influence of cellular metabolism and immune cell function, highlighting the significance of metabolic reprogramming in immune cell activation and effector functions. Metabolic processes such as glycolysis, oxidative phosphorylation, and fatty acid oxidation have been shown to undergo dynamic changes during immune cell response, facilitating the energetic and biosynthetic demands. This review aims to provide a better understanding of the metabolic reprogramming that occurs in different immune cells upon activation, with a special focus on central nervous system disorders. Understanding the metabolic changes of the immune response not only provides insights into the fundamental mechanisms that regulate immune cell function but also opens new approaches for therapeutic strategies aimed at manipulating the immune system.
    Language English
    Publishing date 2023-12-21
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.391330
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  8. Article ; Online: Introduction to the interleukin-1 family of cytokines and receptors: Drivers of innate inflammation and acquired immunity.

    Dinarello, Charles A

    Immunological reviews

    2017  Volume 281, Issue 1, Page(s) 5–7

    MeSH term(s) Adaptive Immunity/immunology ; Animals ; B-Lymphocytes/immunology ; Humans ; Immunity, Innate/immunology ; Inflammation/immunology ; Interleukin-1/immunology ; Receptors, Interleukin-1/immunology ; T-Lymphocytes/immunology
    Chemical Substances Interleukin-1 ; Receptors, Interleukin-1
    Language English
    Publishing date 2017-12-18
    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.12624
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    In stock of ZB MED Cologne/Königswinter

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  9. Article ; Online: Overview of the IL-1 family in innate inflammation and acquired immunity.

    Dinarello, Charles A

    Immunological reviews

    2017  Volume 281, Issue 1, Page(s) 8–27

    Abstract: The interleukin-1 (IL-1) family of cytokines and receptors is unique in immunology because the IL-1 family and Toll-like receptor (TLR) families share similar functions. More than any other cytokine family, the IL-1 family is primarily associated with ... ...

    Abstract The interleukin-1 (IL-1) family of cytokines and receptors is unique in immunology because the IL-1 family and Toll-like receptor (TLR) families share similar functions. More than any other cytokine family, the IL-1 family is primarily associated with innate immunity. More than 95% of living organisms use innate immune mechanisms for survival whereas less than 5% depend on T- and B-cell functions. Innate immunity is manifested by inflammation, which can function as a mechanism of host defense but when uncontrolled is detrimental to survival. Each member of the IL-1 receptor and TLR family contains the cytoplasmic Toll-IL-1-Receptor (TIR) domain. The 50 amino acid TIR domains are highly homologous with the Toll protein in Drosophila. The TIR domain is nearly the same and present in each TLR and each IL-1 receptor family. Whereas IL-1 family cytokine members trigger innate inflammation via IL-1 family of receptors, TLRs trigger inflammation via bacteria, microbial products, viruses, nucleic acids, and damage-associated molecular patterns (DAMPs). In fact, IL-1 family member IL-1a and IL-33 also function as DAMPs. Although the inflammatory properties of the IL-1 family dominate in innate immunity, IL-1 family member can play a role in acquired immunity. This overview is a condensed update of the IL-1 family of cytokines and receptors.
    MeSH term(s) Adaptive Immunity ; Animals ; Drosophila ; Humans ; Immunity, Innate ; Inflammation ; Interleukin-1/metabolism ; Interleukin-33/metabolism ; Receptors, Interleukin-1/metabolism ; Toll-Like Receptors/metabolism
    Chemical Substances Interleukin-1 ; Interleukin-33 ; Receptors, Interleukin-1 ; Toll-Like Receptors
    Language English
    Publishing date 2017-12-15
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/imr.12621
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  10. Article ; Online: Editorial: Cytokines and Intestinal Mucosal Immunity.

    Pizarro, Theresa T / Dinarello, Charles A / Cominelli, Fabio

    Frontiers in immunology

    2021  Volume 12, Page(s) 698693

    MeSH term(s) Animals ; Cytokines/immunology ; Humans ; Immunity, Mucosal/immunology ; Intestinal Mucosa/immunology
    Chemical Substances Cytokines
    Language English
    Publishing date 2021-05-14
    Publishing country Switzerland
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.698693
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