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  1. Article ; Online: Immunoregulatory natural killer cells.

    Roe, Kevin

    Clinica chimica acta; international journal of clinical chemistry

    2024  , Page(s) 117896

    Abstract: This review discusses a broader scope of functional roles for NK cells. Despite the well-known cytolytic and inflammatory roles of NK cells against tumors and pathogenic diseases, extensive evidence demonstrates certain subsets of NK cells have defacto ... ...

    Abstract This review discusses a broader scope of functional roles for NK cells. Despite the well-known cytolytic and inflammatory roles of NK cells against tumors and pathogenic diseases, extensive evidence demonstrates certain subsets of NK cells have defacto immunoregulatory effects and have a role in inducing anergy or lysis of antigen-activated T cells and regulating several autoimmune diseases. Furthermore, recent evidence suggests certain subsets of immunoregulatory NK cells can cause anergy or lysis of antigen-activated T cells to regulate hyperinflammatory diseases, including multisystem inflammatory syndrome. Several pathogens induce T cell and NK cell exhaustion and/or suppression, which impair the immune system's control of the replication speed of virulent pathogens and tumors and result in extensive antigens and antigen-antibody immune complexes, potentially inducing a Type III hypersensitivity immune reaction. The Type III hypersensitivity immune reaction induces immune cell secretion of proteinases, which can create autoantigens which activate T cells to initiate autoimmune and/or hyperinflammatory diseases. Furthermore, pathogen induced NK cell exhaustion and/or suppression will inhibit NK cells which would have induced the anergy or lysis of activated T cells to regulate autoimmune and hyperinflammatory diseases. Autoimmune and hyperinflammatory diseases can be consequences of the dual lymphocyte exhaustion and/or suppression effects during infections, by creating autoimmune and/or hyperinflammatory diseases, while also impairing lymphocytes which would have regulated these diseases.
    Language English
    Publishing date 2024-04-05
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 80228-1
    ISSN 1873-3492 ; 0009-8981
    ISSN (online) 1873-3492
    ISSN 0009-8981
    DOI 10.1016/j.cca.2024.117896
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Correction to: A latent pathogen infection classification system that would significantly increase healthcare safety.

    Roe, Kevin

    Immunologic research

    2023  Volume 71, Issue 5, Page(s) 678

    Language English
    Publishing date 2023-04-25
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 632857-x
    ISSN 1559-0755 ; 0257-277X
    ISSN (online) 1559-0755
    ISSN 0257-277X
    DOI 10.1007/s12026-023-09386-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The interferon-stimulated genes are plausibly a primary genetic locus for genetically enabling hyperinflammatory and autoimmune diseases and lymphocyte exhaustion.

    Roe, Kevin

    Human cell

    2023  Volume 36, Issue 6, Page(s) 2278–2280

    Language English
    Publishing date 2023-08-25
    Publishing country Japan
    Document type Letter
    ZDB-ID 1149134-6
    ISSN 1749-0774 ; 0914-7470
    ISSN (online) 1749-0774
    ISSN 0914-7470
    DOI 10.1007/s13577-023-00969-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Hyperinflammatory disease and vasculitis-associated autoimmune disease pathogenesis by novel virulent pathogens inducing lymphocyte exhaustion and/or suppression.

    Roe, Kevin

    Human cell

    2023  Volume 36, Issue 2, Page(s) 872–874

    MeSH term(s) Humans ; Autoimmune Diseases ; Vasculitis/etiology ; Vasculitis/pathology ; Lymphocytes/pathology
    Language English
    Publishing date 2023-01-24
    Publishing country Japan
    Document type Letter
    ZDB-ID 1149134-6
    ISSN 1749-0774 ; 0914-7470
    ISSN (online) 1749-0774
    ISSN 0914-7470
    DOI 10.1007/s13577-023-00862-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: A latent pathogen infection classification system that would significantly increase healthcare safety.

    Roe, Kevin

    Immunologic research

    2023  Volume 71, Issue 5, Page(s) 673–677

    Abstract: Most viral, bacterial, fungal, and protozoan pathogens can cause latent infections. Latent pathogens can be reactivated from any intentional medical treatment causing immune system suppression, pathogen infections, malnutrition, stress, or drug side ... ...

    Abstract Most viral, bacterial, fungal, and protozoan pathogens can cause latent infections. Latent pathogens can be reactivated from any intentional medical treatment causing immune system suppression, pathogen infections, malnutrition, stress, or drug side effects. These reactivations of latent pathogen infections can be dangerous and even lethal, especially in immuno-suppressed individuals. The latent pathogen infections in an individual can be classified and updated on a periodic basis in a four category system by whether or not an individual's immune system is damaged and by whether or not these latent infections will assist other active or latent pathogen infections. Such a classification system for latent infections by viral, bacterial, fungal, and protozoan parasite pathogens would be practical and useful and indicate whether certain medical treatments will be dangerous for transmitting or reactivating an individual's latent pathogen infections. This classification system will immediately provide latent pathogen infection status information that is potentially vital for emergency care and essential for quickly and safely selecting tissue or organ transplant donors and recipients, and it will significantly increase the safety of medical care for both patients and medical care providers.
    MeSH term(s) Humans ; Latent Infection ; Delivery of Health Care
    Language English
    Publishing date 2023-04-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 632857-x
    ISSN 1559-0755 ; 0257-277X
    ISSN (online) 1559-0755
    ISSN 0257-277X
    DOI 10.1007/s12026-023-09377-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Treatment alternatives for multidrug-resistant fungal pathogens.

    Roe, Kevin

    Drug discovery today

    2023  Volume 28, Issue 6, Page(s) 103596

    Abstract: Several fungal pathogens are becoming resistant to conventional fungal infection treatments, and some fungal pathogens have become multidrug-resistant. Alternative treatments include fungal vaccines, conventional or synthetic monoclonal antibody (mAb) ... ...

    Abstract Several fungal pathogens are becoming resistant to conventional fungal infection treatments, and some fungal pathogens have become multidrug-resistant. Alternative treatments include fungal vaccines, conventional or synthetic monoclonal antibody (mAb) injections, or potentially conventional or synthetic mAbs produced in vivo by injections of appropriately packaged mRNA. Specifically synthesized proteins can mask distinctive pathogenic fungal surface proteins and target pathogenic fungal proteins to stop fungal infections. Treatments could also use combinations of one or more antifungal drugs combined with direct injections or injections of packaged mRNA with instructions for patient synthesis of either the conventional or synthetic mAbs. These alternative treatments offer potentially significant advantages compared with existing treatments for fungal pathogens.
    MeSH term(s) Humans ; Fungi ; Antifungal Agents/pharmacology ; Antifungal Agents/therapeutic use ; Mycoses/drug therapy ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use
    Chemical Substances Antifungal Agents ; Antibodies, Monoclonal
    Language English
    Publishing date 2023-04-20
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1324988-5
    ISSN 1878-5832 ; 1359-6446
    ISSN (online) 1878-5832
    ISSN 1359-6446
    DOI 10.1016/j.drudis.2023.103596
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Eight influenza virus cellular manipulations which can boost concurrent SARS-CoV-2 infections to severe outcomes.

    Roe, Kevin

    Human cell

    2023  Volume 36, Issue 5, Page(s) 1581–1592

    Abstract: Viral pathogens in the lungs can cause severe outcomes, including acute lung injury and acute respiratory distress syndrome. Dangerous respiratory pathogens include some influenza A and B viruses, and the severe acute respiratory syndrome coronavirus 2 ( ... ...

    Abstract Viral pathogens in the lungs can cause severe outcomes, including acute lung injury and acute respiratory distress syndrome. Dangerous respiratory pathogens include some influenza A and B viruses, and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Unfortunately, concurrent infections of influenza virus and SARS-CoV-2 increase severe outcome probabilities. Influenza viruses have eight cellular manipulations which can assist concurrent SARS-CoV-2 viral infections. The eight cellular manipulations include: (1) viral protein binding with cellular sensors to block antiviral transcription factors and cytokine expressions, (2) viral protein binding with cell proteins to impair cellular pre-messenger ribonucleic acid splicing, (3) increased ribonucleic acid virus replication through the phosphatidylinositol 3-kinase/Akt (protein kinase B) pathway, (4) regulatory ribonucleic acids to manipulate cellular sensors and pathways to suppress antiviral defenses, (5) exosomes to transmit influenza virus to uninfected cells to weaken cellular defenses before SARS-CoV-2 infection, (6) increased cellular cholesterol and lipids to improve virion synthesis stability, quality and virion infectivity, (7) increased cellular autophagy, benefiting influenza virus and SARS-CoV-2 replications and (8) adrenal gland stimulation to produce glucocorticoids, which suppress immune cells, including reduced synthesis of cytokines, chemokines and adhesion molecules. Concurrent infections by one of the influenza viruses and SARS-CoV-2 will increase the probability of severe outcomes, and with sufficient synergy potentially enable the recurrence of tragic pandemics.
    MeSH term(s) Humans ; COVID-19 ; SARS-CoV-2 ; Virus Replication ; Cytokines ; Antiviral Agents ; Orthomyxoviridae ; RNA
    Chemical Substances Cytokines ; Antiviral Agents ; RNA (63231-63-0)
    Language English
    Publishing date 2023-06-12
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 1149134-6
    ISSN 1749-0774 ; 0914-7470
    ISSN (online) 1749-0774
    ISSN 0914-7470
    DOI 10.1007/s13577-023-00923-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Deadly interactions: Synergistic manipulations of concurrent pathogen infections potentially enabling future pandemics.

    Roe, Kevin

    Drug discovery today

    2023  Volume 28, Issue 11, Page(s) 103762

    Abstract: Certain mono-infections of influenza viruses and novel coronaviruses, including severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) are significant threats to human health. Concurrent infections by influenza viruses and coronaviruses increases ... ...

    Abstract Certain mono-infections of influenza viruses and novel coronaviruses, including severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) are significant threats to human health. Concurrent infections by influenza viruses and coronaviruses increases their danger. Influenza viruses have eight manipulations capable of assisting SARS-CoV-2 and other coronaviruses, and several of these manipulations, which are not specific to viruses, can also directly or indirectly boost dangerous secondary bacterial pneumonias. The influenza virus manipulations include: inhibiting transcription factors and cytokine expression; impairing defensive protein expression; increasing RNA viral replication; inhibiting defenses by manipulating cellular sensors and signaling pathways; inhibiting defenses by secreting exosomes; stimulating cholesterol production to increase synthesized virion infectivities; increasing cellular autophagy to assist viral replication; and stimulating glucocorticoid synthesis to suppress innate and adaptive immune defenses by inhibiting cytokine, chemokine, and adhesion molecule production. Teaser: Rapidly spreading multidrug-resistant respiratory bacteria, combined with influenza virus's far-reaching cellular defense manipulations benefiting evolving SARS-CoV-2 or other coronaviruses and/or respiratory bacteria, can enable more severe pandemics or co-pandemics.
    MeSH term(s) Humans ; COVID-19 ; Pandemics ; SARS-CoV-2 ; Influenza, Human ; Cytokines
    Chemical Substances Cytokines
    Language English
    Publishing date 2023-09-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 1324988-5
    ISSN 1878-5832 ; 1359-6446
    ISSN (online) 1878-5832
    ISSN 1359-6446
    DOI 10.1016/j.drudis.2023.103762
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: A mammalian lung's immune system minimizes tissue damage by initiating five major sequential phases of defense.

    Roe, Kevin

    Clinical and experimental medicine

    2023  Volume 23, Issue 7, Page(s) 2967–2977

    Abstract: The mammalian lungs encounter several pathogens, but have a sophisticated multi-phase immune defense. Furthermore, several immune responses to suppress pulmonary pathogens can damage the airway epithelial cells, particularly the vital alveolar epithelial ...

    Abstract The mammalian lungs encounter several pathogens, but have a sophisticated multi-phase immune defense. Furthermore, several immune responses to suppress pulmonary pathogens can damage the airway epithelial cells, particularly the vital alveolar epithelial cells (pneumocytes). The lungs have a sequentially activated, but overlapping, five phase immune response to suppress most pathogens, while causing minimal damage to the airway epithelial cells. Each phase of the immune response may suppress the pathogens, but if the previous phase proves inadequate, a stronger phase of immune response is activated, but with an increased risk of airway epithelial cell damage. The first phase immune response involves the pulmonary surfactants, which have proteins and phospholipids with potentially sufficient antibacterial, antifungal and antiviral properties to suppress many pathogens. The second phase immune response involves the type III interferons, having pathogen responses with comparatively minimal risk of damage to airway epithelial cells. The third phase immune response involves type I interferons, which implement stronger immune responses against pathogens with an increased risk of damage to airway epithelial cells. The fourth phase immune response involves the type II interferon, interferon-γ, which activates stronger immune responses, but with considerable risk of airway epithelial cell damage. The fifth phase immune response involves antibodies, potentially activating the complement system. In summary, five major phases of immune responses for the lungs are sequentially initiated to create an overlapping immune response which can suppress most pathogens, while usually causing minimal damage to the airway epithelial cells, including the pneumocytes.
    MeSH term(s) Animals ; Humans ; Interferons ; Lung ; Epithelial Cells ; Immune System ; Interferon Lambda ; Mammals/metabolism
    Chemical Substances Interferons (9008-11-1) ; Interferon Lambda
    Language English
    Publishing date 2023-05-04
    Publishing country Italy
    Document type Journal Article ; Review
    ZDB-ID 2053018-3
    ISSN 1591-9528 ; 1591-8890
    ISSN (online) 1591-9528
    ISSN 1591-8890
    DOI 10.1007/s10238-023-01083-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Increased Fungal Infection Mortality Induced by Concurrent Viral Cellular Manipulations.

    Roe, Kevin

    Lung

    2023  Volume 201, Issue 5, Page(s) 467–476

    Abstract: Certain respiratory fungal pathogen mono-infections can cause high mortality rates. Several viral pathogen mono-infections, including influenza viruses and coronaviruses including SARS-CoV-2, can also cause high mortality rates. Concurrent infections by ... ...

    Abstract Certain respiratory fungal pathogen mono-infections can cause high mortality rates. Several viral pathogen mono-infections, including influenza viruses and coronaviruses including SARS-CoV-2, can also cause high mortality rates. Concurrent infections by fungal pathogens and highly manipulative viral pathogens can synergistically interact in the respiratory tract to substantially increase their mortality rates. There are at least five viral manipulations which can assist secondary fungal infections. These viral manipulations include the following: (1) inhibiting transcription factors and cytokine expressions, (2) impairing defensive protein expressions, (3) inhibiting defenses by manipulating cellular sensors and signaling pathways, (4) inhibiting defenses by secreting exosomes, and (5) stimulating glucocorticoid synthesis to suppress immune defenses by inhibiting cytokine, chemokine, and adhesion molecule production. The highest mortality respiratory viral pandemics up to now have had substantially boosted mortalities by inducing secondary bacterial pneumonias. However, numerous animal species besides humans are also carriers of endemic infections by viral and multidrug-resistant fungal pathogens. The vast multi-species scope of endemic infection opportunities make it plausible that the pro-fungal manipulations of a respiratory virus can someday evolve to enable a very high mortality rate viral pandemic inducing multidrug-resistant secondary fungal pathogen infections. Since such pandemics can quickly spread world-wide and outrun existing treatments, it would be worthwhile to develop new antifungal treatments well before such a high mortality event occurs.
    MeSH term(s) Humans ; Animals ; SARS-CoV-2 ; COVID-19 ; Respiratory Tract Infections/microbiology ; Mycoses/epidemiology ; Cytokines
    Chemical Substances Cytokines
    Language English
    Publishing date 2023-09-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 6165-7
    ISSN 1432-1750 ; 0341-2040
    ISSN (online) 1432-1750
    ISSN 0341-2040
    DOI 10.1007/s00408-023-00642-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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