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  1. Article ; Online: MIF contribution to progressive brain diseases.

    Matejuk, Agata / Benedek, Gil / Bucala, Richard / Matejuk, Szymon / Offner, Halina / Vandenbark, Arthur A

    Journal of neuroinflammation

    2024  Volume 21, Issue 1, Page(s) 8

    Abstract: Progressive brain diseases create a huge social and economic burden on modern societies as a major cause of disability and death. Incidence of brain diseases has a significantly increasing trend and merits new therapeutic strategies. At the base of many ... ...

    Abstract Progressive brain diseases create a huge social and economic burden on modern societies as a major cause of disability and death. Incidence of brain diseases has a significantly increasing trend and merits new therapeutic strategies. At the base of many progressive brain malfunctions is a process of unresolved, chronic inflammation. Macrophage migration inhibitory factor, MIF, is an inflammatory mediator that recently gained interest of neuro-researchers due to its varied effects on the CNS such as participation of nervous system development, neuroendocrine functions, and modulation of neuroinflammation. MIF appears to be a candidate as a new biomarker and target of novel therapeutics against numerous neurologic diseases ranging from cancer, autoimmune diseases, vascular diseases, neurodegenerative pathology to psychiatric disorders. In this review, we will focus on MIF's crucial role in neurological diseases such as multiple sclerosis (MS), Alzheimer's disease (AD) and glioblastoma (GBM).
    MeSH term(s) Humans ; Macrophage Migration-Inhibitory Factors/genetics ; Inflammation ; Multiple Sclerosis ; Calgranulin A ; Calgranulin B ; Nervous System Diseases ; Brain Diseases ; Intramolecular Oxidoreductases
    Chemical Substances Macrophage Migration-Inhibitory Factors ; Calgranulin A ; Calgranulin B ; MIF protein, human (EC 5.3.2.1) ; Intramolecular Oxidoreductases (EC 5.3.-)
    Language English
    Publishing date 2024-01-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-023-02993-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Modeling immunity and inflammation in stroke: don't be afraid of mice?

    Offner, Halina

    Stroke

    2014  Volume 45, Issue 9, Page(s) e181–2

    MeSH term(s) Animals ; Female ; Genomics ; Humans ; Inflammation/genetics ; Male
    Language English
    Publishing date 2014-07-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80381-9
    ISSN 1524-4628 ; 0039-2499 ; 0749-7954
    ISSN (online) 1524-4628
    ISSN 0039-2499 ; 0749-7954
    DOI 10.1161/STROKEAHA.114.005642
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 448: Show issues Location:
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  3. Article ; Online: Novel therapeutic for multiple sclerosis protects white matter function in EAE mouse model.

    Zerimech, Sarah / Nguyen, Hung / Vandenbark, Arthur A / Offner, Halina / Baltan, Selva

    Frontiers in molecular medicine

    2023  Volume 3

    Abstract: Multiple sclerosis (MS) is a chronic demyelinating disease with prominent axon dysfunction. Our previous studies in an MS mouse model, experimental autoimmune encephalomyelitis (EAE), demonstrated that major histocompatibility complex Class II constructs ...

    Abstract Multiple sclerosis (MS) is a chronic demyelinating disease with prominent axon dysfunction. Our previous studies in an MS mouse model, experimental autoimmune encephalomyelitis (EAE), demonstrated that major histocompatibility complex Class II constructs can reverse clinical signs of EAE. These constructs block binding and downstream signaling of macrophage migration inhibitory factors (MIF-1/2) through CD74, thereby inhibiting phosphorylation of extracellular signal-regulated kinase (ERK) activation and tissue inflammation and promoting remyelination. To directly assess the effects of a novel third generation construct, DRhQ, on axon integrity in EAE, we compared axon conduction properties using electrophysiology on corpus callosum slices and optic nerves. By using two distinct white matter (WM) tracts, we aimed to assess the impact of the EAE and the benefit of DRhQ on myelinated and unmyelinated axons as well as to test the clinical value of DRhQ on demyelinating lesions in CC and optic myelitis. Our study found that EAE altered axon excitability, delayed axon conduction and slowed spatiotemporal summation correlated with diffuse astrocyte and microglia activation. Because MS predisposes patients to stroke, we also investigated and showed that vulnerability to WM ischemia is increased in the EAE MS mouse model. Treatment with DRhQ after the onset of EAE drastically inhibited microglial and astrocyte activation, improved functional integrity of the myelinated axons and enhanced recovery after ischemia. These results demonstrate that DRhQ administered after the onset of EAE promotes WM integrity and function, and reduces subsequent vulnerability to ischemic injury, suggesting important therapeutic potential for treatment of progressive MS.
    Language English
    Publishing date 2023-08-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 3123823-3
    ISSN 2674-0095 ; 2674-0095
    ISSN (online) 2674-0095
    ISSN 2674-0095
    DOI 10.3389/fmmed.2023.1237078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Cross-Talk of the CNS With Immune Cells and Functions in Health and Disease.

    Matejuk, Agata / Vandenbark, Arthur A / Offner, Halina

    Frontiers in neurology

    2021  Volume 12, Page(s) 672455

    Abstract: The immune system's role is much more than merely recognizing self vs. non-self and involves maintaining homeostasis and integrity of the organism starting from early development to ensure proper organ function later in life. Unlike other systems, the ... ...

    Abstract The immune system's role is much more than merely recognizing self vs. non-self and involves maintaining homeostasis and integrity of the organism starting from early development to ensure proper organ function later in life. Unlike other systems, the central nervous system (CNS) is separated from the peripheral immune machinery that, for decades, has been envisioned almost entirely as detrimental to the nervous system. New research changes this view and shows that blood-borne immune cells (both adaptive and innate) can provide homeostatic support to the CNS via neuroimmune communication. Neurodegeneration is mostly viewed through the lens of the resident brain immune populations with little attention to peripheral circulation. For example, cognition declines with impairment of peripheral adaptive immunity but not with the removal of microglia. Therapeutic failures of agents targeting the neuroinflammation framework (inhibiting immune response), especially in neurodegenerative disorders, call for a reconsideration of immune response contributions. It is crucial to understand cross-talk between the CNS and the immune system in health and disease to decipher neurodestructive and neuroprotective immune mechanisms for more efficient therapeutic strategies.
    Language English
    Publishing date 2021-05-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2021.672455
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: PD-L1 is required for estrogen-induced protection against severe EAE in IL-10 deficient mice

    Offner, Halina / Lockwood, Denesa / Meza-Romero, Roberto / Vandenbark, Arthur A

    Metabolic brain disease

    2022  Volume 38, Issue 2, Page(s) 589–599

    Abstract: Background: IL-10 knockout (KO) mice can be protected against experimental autoimmune encephalomyelitis (EAE) with low-dose estrogen (E2) treatment similar to wild type (WT) mice, indicating that IL-10 is not required for E2-induced EAE protection. Our ... ...

    Abstract Background: IL-10 knockout (KO) mice can be protected against experimental autoimmune encephalomyelitis (EAE) with low-dose estrogen (E2) treatment similar to wild type (WT) mice, indicating that IL-10 is not required for E2-induced EAE protection. Our previous study demonstrated that E2 treatment induced an increase in programmed death ligands 1 (PD-L1) and 2 (PD-L2) on monocytes and macrophages in the periphery and within the CNS. In this study, we selectively inhibited the function of PD-L1 and PD-L2 to evaluate their critical role in maintaining E2-induced protection against EAE in IL-10-KO mice.
    Methods: This study used female IL-10 KO mice pre-treated with either E2 or sham pellets seven days prior to induction of EAE and subsequently treated with Vehicle or antibodies to PD-L1, PD-L2 or respective isotype controls. Mice were scored daily for EAE severity over 21 days post-EAE induction. Cells from the spleen and brain were evaluated by flow cytometry.
    Results: Differences in EAE severity were assessed in E2 and sham pre-treated IL-10-KO mice treated with α-PD-L1 or α-PD-L2 antibodies over the course of disease compared to treatment with Vehicle or isotype control antibodies. The results revealed real-time development of severe EAE in E2-pre-treated IL-10-KO mice treated with α-PD-L1 but not α-PD-L2 antibodies, mediated in part by increased percentages of activated CD74
    Conclusion: These results demonstrate unequivocally that PD-L1 but not PD-L2 was required to retain the inhibitory effects of E2 on clinical EAE scores in female IL-10-KO mice and further implicate the emergence of the MIF/CD74 axis as a contributing pathogenic mechanism.
    MeSH term(s) Animals ; Female ; Mice ; B7-H1 Antigen ; Brain ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Estrogens/pharmacology ; Interleukin-10 ; Mice, Inbred C57BL ; Mice, Knockout
    Chemical Substances B7-H1 Antigen ; Estrogens ; Interleukin-10 (130068-27-8) ; Cd274 protein, mouse ; IL10 protein, mouse
    Language English
    Publishing date 2022-12-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 632824-6
    ISSN 1573-7365 ; 0885-7490
    ISSN (online) 1573-7365
    ISSN 0885-7490
    DOI 10.1007/s11011-022-01129-8
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2155: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article ; Online: Surviving the storm: Dealing with COVID-19.

    Vandenbark, Arthur A / Meza-Romero, Roberto / Offner, Halina

    Cellular immunology

    2020  Volume 354, Page(s) 104153

    MeSH term(s) Anti-Inflammatory Agents/pharmacology ; Antigens, Differentiation, B-Lymphocyte/immunology ; Antigens, Differentiation, B-Lymphocyte/metabolism ; Betacoronavirus/physiology ; COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Coronavirus Infections/pathology ; Cytokine Release Syndrome/drug therapy ; Cytokine Release Syndrome/pathology ; HLA-DR alpha-Chains/genetics ; Histocompatibility Antigens Class II/immunology ; Histocompatibility Antigens Class II/metabolism ; Humans ; Myelin-Oligodendrocyte Glycoprotein/genetics ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/immunology ; Pneumonia, Viral/pathology ; Receptors, Antigen, T-Cell/antagonists & inhibitors ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Recombinant Proteins/pharmacology ; SARS-CoV-2
    Chemical Substances Anti-Inflammatory Agents ; Antigens, Differentiation, B-Lymphocyte ; DRhQ ; HLA-DR alpha-Chains ; Histocompatibility Antigens Class II ; MOG protein, human ; Myelin-Oligodendrocyte Glycoprotein ; Receptors, Antigen, T-Cell ; Recombinant Proteins ; invariant chain
    Keywords covid19
    Language English
    Publishing date 2020-06-13
    Publishing country Netherlands
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80094-6
    ISSN 1090-2163 ; 0008-8749
    ISSN (online) 1090-2163
    ISSN 0008-8749
    DOI 10.1016/j.cellimm.2020.104153
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 417: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  7. Article ; Online: Microglia and astrocyte involvement in neurodegeneration and brain cancer.

    Vandenbark, Arthur A / Offner, Halina / Matejuk, Szymon / Matejuk, Agata

    Journal of neuroinflammation

    2021  Volume 18, Issue 1, Page(s) 298

    Abstract: The brain is unique and the most complex organ of the body, containing neurons and several types of glial cells of different origins and properties that protect and ensure normal brain structure and function. Neurological disorders are the result of a ... ...

    Abstract The brain is unique and the most complex organ of the body, containing neurons and several types of glial cells of different origins and properties that protect and ensure normal brain structure and function. Neurological disorders are the result of a failure of the nervous system multifaceted cellular networks. Although great progress has been made in the understanding of glia involvement in neuropathology, therapeutic outcomes are still not satisfactory. Here, we discuss recent perspectives on the role of microglia and astrocytes in neurological disorders, including the two most common neurodegenerative conditions, Alzheimer disease and progranulin-related frontotemporal lobar dementia, as well as astrocytoma brain tumors. We emphasize key factors of microglia and astrocytic biology such as the highly heterogeneic glial nature strongly dependent on the environment, genetic factors that predispose to certain pathologies and glia senescence that inevitably changes the CNS landscape. Our understanding of diverse glial contributions to neurological diseases can lead advances in glial biology and their functional recovery after CNS malfunction.
    MeSH term(s) Animals ; Astrocytes/pathology ; Brain Neoplasms/complications ; Brain Neoplasms/pathology ; Humans ; Microglia/pathology ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/pathology
    Language English
    Publishing date 2021-12-23
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-021-02355-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The splenic response to stroke: from rodents to stroke subjects.

    Seifert, Hilary A / Offner, Halina

    Journal of neuroinflammation

    2018  Volume 15, Issue 1, Page(s) 195

    Abstract: Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in ... ...

    Abstract Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in lower- and middle-income countries compared to high-income countries. The role of the spleen in stroke has been studied in rodent models of stroke and is seen as a major contributor to increased secondary neural injury after stroke. Splenectomy 2 weeks prior to ischemic and hemorrhagic stroke in mice and rats shows decreased infarct volumes. Additionally, the spleen decreases in size following stroke in rodents. Pro-inflammatory mediators are also increased in the spleen and subsequently the brain after stroke. These data in preclinical models of stroke have led stroke neurologists to look at the splenic response in stroke subjects. The outcomes of these studies suggest the spleen is responding in a similar manner in stroke subjects as it is in animal models of stroke.
    Conclusion: Animal models demonstrating the detrimental role of the spleen in stroke are providing strong evidence of how the spleen is responding during stroke in human subjects. This indicates treatments targeting the splenic immune response in animals could provide useful targets and treatments for stroke subjects.
    MeSH term(s) Animals ; Disease Models, Animal ; Humans ; Mice ; Rats ; Spleen/physiology ; Splenectomy ; Stroke/immunology ; Stroke/pathology
    Language English
    Publishing date 2018-07-03
    Publishing country England
    Document type Journal Article ; Review
    ISSN 1742-2094
    ISSN (online) 1742-2094
    DOI 10.1186/s12974-018-1239-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Surviving the storm

    Vandenbark, Arthur A. / Meza-Romero, Roberto / Offner, Halina

    Cellular Immunology

    Dealing with COVID-19

    2020  Volume 354, Page(s) 104153

    Keywords Immunology ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 80094-6
    ISSN 1090-2163 ; 0008-8749
    ISSN (online) 1090-2163
    ISSN 0008-8749
    DOI 10.1016/j.cellimm.2020.104153
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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