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  • 1
    Online Resource
    Online Resource
    Stress-elicited glucocorticoid receptor signaling upregulates TIGIT in innate-like invariant T lymphocytes
    Elsevier BV ; 2019
    In:  Brain, Behavior, and Immunity Vol. 80 ( 2019-08), p. 793-804
    Details
    In: Brain, Behavior, and Immunity, Elsevier BV, Vol. 80 ( 2019-08), p. 793-804
    Type of Medium: Online Resource
    ISSN: 0889-1591
    URL: Article
    DOI: 10.1016/j.bbi.2019.05.027
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 1462491-6
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  • 2
    Online Resource
    Online Resource
    Editorial: CD1- and MR1-Restricted T Cells in Antimicrobial Immunity
    Frontiers Media SA ; 2015
    In:  Frontiers in Immunology Vol. 6 ( 2015-12-02)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 6 ( 2015-12-02)
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2015.00611
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2015
    detail.hit.zdb_id: 2606827-8
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  • 3
    Online Resource
    Online Resource
    B cell-T cell interplay in immune regulation: A focus on follicular regulatory T and regulatory B cell functions
    Frontiers Media SA ; 2022
    In:  Frontiers in Cell and Developmental Biology Vol. 10 ( 2022-9-23)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 10 ( 2022-9-23)
    Abstract: B cells are the core components of humoral immunity. A mature B cell can serve in multiple capacities, including antibody production, antigen presentation, and regulatory functions. Forkhead box P3 (FoxP3)-expressing regulatory T cells (Tregs) are key players in sustaining immune tolerance and keeping inflammation in check. Mounting evidence suggests complex communications between B cells and Tregs. In this review, we summarize the yin-yang regulatory relationships between B cells and Tregs mainly from the perspectives of T follicular regulatory (Tfr) cells and regulatory B cells (Bregs). We discuss the regulatory effects of Tfr cells on B cell proliferation and the germinal center response. Additionally, we review the indispensable role of B cells in ensuring homeostatic Treg survival and describe the function of Bregs in promoting Treg responses. Finally, we introduce a new subset of Tregs, termed Treg-of-B cells, which are induced by B cells, lake the expression of FoxP3 but still own immunomodulatory effects. In this article, we also enumerate a sequence of research from clinical patients and experimental models to clarify the role of Tfr cells in germinal centers and the role of convention B cells and Bregs to Tregs in the context of different diseases. This review offers an updated overview of immunoregulatory networks and unveils potential targets for therapeutic interventions against cancer, autoimmune diseases and allograft rejection.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    DOI: 10.3389/fcell.2022.991840
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2737824-X
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  • 4
    Online Resource
    Online Resource
    Identification of poxvirus CD8+ T cell determinants to enable rational design and characterization of smallpox vaccines
    Rockefeller University Press ; 2005
    In:  The Journal of Experimental Medicine Vol. 201, No. 1 ( 2005-01-03), p. 95-104
    Details
    In: The Journal of Experimental Medicine, Rockefeller University Press, Vol. 201, No. 1 ( 2005-01-03), p. 95-104
    Abstract: The large size of poxvirus genomes has stymied attempts to identify determinants recognized by CD8+ T cells and greatly impeded development of mouse smallpox vaccination models. Here, we use a vaccinia virus (VACV) expression library containing each of the predicted 258 open reading frames to identify five peptide determinants that account for approximately half of the VACV-specific CD8+ T cell response in C57BL/6 mice. We show that the primary immunodominance hierarchy is greatly affected by the route of VACV infection and the poxvirus strain used. Modified vaccinia virus ankara (MVA), a candidate replacement smallpox vaccine, failed to induce responses to two of the defined determinants. This could not be predicted by genomic comparison of viruses and is not due strictly to limited MVA replication in mice. Several determinants are immunogenic in cowpox and ectromelia (mousepox) virus infections, and immunization with the immunodominant determinant provided significant protection against lethal mousepox. These findings have important implications for understanding poxvirus immunity in animal models and bench-marking immune responses to poxvirus vaccines in humans.
    Type of Medium: Online Resource
    ISSN: 1540-9538 , 0022-1007
    URL: Article
    DOI: 10.1084/jem.20041912
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2005
    detail.hit.zdb_id: 1477240-1
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  • 5
    Online Resource
    Online Resource
    NKT cell costimulation: experimental progress and therapeutic promise
    Elsevier BV ; 2011
    In:  Trends in Molecular Medicine Vol. 17, No. 2 ( 2011-2), p. 65-77
    Details
    In: Trends in Molecular Medicine, Elsevier BV, Vol. 17, No. 2 ( 2011-2), p. 65-77
    Type of Medium: Online Resource
    ISSN: 1471-4914
    URL: Article
    DOI: 10.1016/j.molmed.2010.10.007
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
    detail.hit.zdb_id: 2155736-6
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Psychological stress triggers the accumulation of myeloid-derived suppressor cells in the liver through adrenergic receptor signaling
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 1_Supplement ( 2023-05-01), p. 167.13-167.13
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 1_Supplement ( 2023-05-01), p. 167.13-167.13
    Abstract: Chronic physiological stress affects tightly regulated crosstalk between the nervous and the immune system. However, the exact mechanism(s) of stress-induced immunomodulation is far from clear. Immature myeloid cells such as myeloid-derived suppressor cells (MDSCs) impair immune responses, which may in turn increase susceptibility to infections and cancer or their complications. In a mouse model of chronic psychological stress through physical restraint, we found mononuclear-MDSC (Mo-MDSC) cells, defined as CD11b +Ly6C highLy6G highcells, to accumulate in the liver. These cells expressed high levels of Mo-MDSC markers such as CD14, TLR4, IL-4Rα as well as markers indicative of anti-apoptotic and immunosuppressive functions (HIF-1α, G-CSFR, Bcl2, Arg2, iNOS). In addition, FACS sorted MDSCs suppressed production of IFN-ɣ by T cells in vitro. Increased levels of proinflammatory mediators were detectable in serum samples of stressed mice, with circulating levels of IL-6 and G-CSF being the most pronounced mediators. The observed intrahepatic accumulation of Mo-MDSC-like cells was mediated by IL-6 and G-CSF and could be reversed by treatment with corresponding receptor-blocking monoclonal antibodies. In addition, this phenomenon was driven by norepinephrine (NE), the main neurotransmitter released from sympathetic neurons, and could be recapitulated by in vivo administration of NE to non-stressed mice. Our work reveals a novel mechanism of immunosuppression that is governed by adrenergic and inflammatory cues and alters the cellular landscape of the liver with implications for immune surveillance against microbes and cancer. This work was funded by NSERC
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.210.Supp.167.13
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    A staphylococcal superantigen unexpectedly augments the response magnitude of cognate anti-influenza CD8+ T cells in mice and humans.
    The American Association of Immunologists ; 2017
    In:  The Journal of Immunology Vol. 198, No. 1_Supplement ( 2017-05-01), p. 203.12-203.12
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 198, No. 1_Supplement ( 2017-05-01), p. 203.12-203.12
    Abstract: Staphylococcal enterotoxin B (SEB) is a bacterial superantigen (SAg) that induces proliferation and inflammatory cytokine secretion by up to 30% of T cells present in one’s repertoire. Eventually, the exposed T cells are thought to undergo activation-induced cell death or anergy, thus creating physical and/or functional holes in the repertoire. Using a mouse model of influenza A virus (IAV) vaccination, we found that primary IAV-specific CD8+ T cell (TCD8+) responses were enhanced, rather than diminished, in SEB-exposed animals. This effect was manifest for both local and systemic responses and validated when several different strains of IAV were utilized. Strikingly, the observed enhancement was easily detectable even one month post-SEB exposure, which was much later than the peak of the anti-IAV response. Importantly, IAV-specific TCD8+ in SEB-primed animals were not only capable of synthesizing interferon (IFN)-γ but also of lysing target cells pulsed with IAV-derived peptides in vivo. Finally, in vitro cultures of human peripheral blood mononuclear cells with SEB revealed that memory TCD8+, which recognize IAV but not Epstein-Barr virus or cytomegalovirus, were specifically expanded by this SAg and persisted long after deletion should have theoretically occurred. Taken together, our findings define a novel phenomenon in the context of TCD8+ responses to SAgs, which has important implications for vaccination against flu in critical care patients afflicted by staphylococcal infections and/or SAg-mediated illnesses.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.198.Supp.203.12
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2017
    detail.hit.zdb_id: 1475085-5
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  • 8
    Online Resource
    Online Resource
    Glucocorticoid receptor signaling during prolonged psychological stress compromises the ability of invariant NKT cells to participate in antitumor immune surveillance
    The American Association of Immunologists ; 2018
    In:  The Journal of Immunology Vol. 200, No. 1_Supplement ( 2018-05-01), p. 57.48-57.48
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 200, No. 1_Supplement ( 2018-05-01), p. 57.48-57.48
    Abstract: The nervous system serves critical roles in the regulation of immune responses. Consequently, the neuroimmune functional interface can be disrupted by psychological stress, potentially impeding our ability to combat malignancies. Invariant natural killer T (iNKT) cells are innate-like T cells that, upon activation by glycolipid antigens and/or select environmental cues such as inflammatory cytokines, participate in antitumor immune responses. However, how mediators of stress may impact iNKT cell functions in this context remains unexplored. We subjected BALB/c and/or C57BL/6 mice to prolonged psychological stress, in a well-established model of physical restraint, before administering α-GalCer (a glycolipid agonist of iNKT cells) or a combination of IL-12 and IL-18. We report that stress abrogates IFN-γ production by activated iNKT cells in vivo, an effect that is reversible by blockade of glucocorticoid receptors. Accordingly, α-GalCer-stimulated iNKT cells in stressed mice failed to protect against pulmonary metastasis of B16-F10 melanoma. We also observed that otherwise α-GalCer-transactivated NK cells from stressed mice had a diminished capacity to lyse YAC-1 lymphoma cells. Finally, the suppressive effect of stress on iNKT cells was not due to their apoptotic death. In fact, unlike conventional T cells, iNKT cells were resistant to glucocorticoid-induced apoptosis. Taken together, our findings define a novel mechanism underlying stress-induced immunosuppression, which involves innate-like but not conventional T lymphocytes.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.200.Supp.57.48
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2018
    detail.hit.zdb_id: 1475085-5
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  • 9
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    Online Resource
    Adenosine acts through an A 3 receptor to prevent the induction of murine anti‐CD3‐activated killer T cells
    Wiley ; 2002
    In:  International Journal of Cancer Vol. 99, No. 3 ( 2002-05-20), p. 386-395
    Details
    In: International Journal of Cancer, Wiley, Vol. 99, No. 3 ( 2002-05-20), p. 386-395
    Abstract: Adenosine, a purine nucleoside found at high levels in solid tumors, is able to suppress the recognition/adhesion and effector phases of killer lymphocyte‐mediated tumor cell destruction. Here, we demonstrate that adenosine, at concentrations that are typically present in the extracellular fluid of solid tumors, exerts a profound inhibitory effect on the induction of mouse cytotoxic T cells, without substantially affecting T‐cell viability. T‐cell proliferation in response to mitogenic anti‐CD3 antibody was impaired in the presence of 10 μM adenosine (plus coformycin to inhibit endogenous adenosine deaminase). Antigen‐specific T‐cell proliferation was similarly inhibited by adenosine. Anti‐CD3‐activated killer T (AK‐T) cells induced in the presence of adenosine exhibited reduced major histocompatibility complex‐unrestricted cytotoxicity against P815 mastocytoma cells in JAM and 51 Cr‐release assays. Diminished tumoricidal activity correlated with reduced expression of mRNAs coding for granzyme B, perforin, Fas ligand and tumor necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL), as well as with diminished N α‐CBZ‐L‐lysine thiobenzylester (BLT) esterase activity. Interleukin‐2 and interferon‐γ synthesis by AK‐T cells was also inhibited by adenosine. AK‐T cells express mRNA coding for A 2A , A 2B and A 3 receptors, but little or no mRNA coding for A 1 receptors. The inhibitory effect of adenosine on AK‐T cell proliferation was blocked by an A 3 receptor antagonist (MRS1191) but not by an A 2 receptor antagonist (3,7‐dimethyl‐1‐propargylxanthine [DMPX]). The A 3 receptor agonists ( N 6 ‐2‐(4‐aminophenyl)ethyladenosine [APNEA] and N 6 ‐benzyl‐5′‐N‐ethylcarboxamidoadenosine [ N 6 ‐benzyl‐NECA]) also inhibited AK‐T cell proliferation. Adenosine, therefore, acts through an A 3 receptor to prevent AK‐T cell induction. Tumor‐associated adenosine may act through the same mechanism to impair the development of tumor‐reactive T cells in cancer patients. © 2002 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v99:3
    DOI: 10.1002/ijc.10325
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 10
    Online Resource
    Online Resource
    Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8〈sup〉+〈/sup〉 T Cell Responses
    MyJove Corporation ; 2019
    In:  Journal of Visualized Experiments , No. 147 ( 2019-05-06)
    Details
    In: Journal of Visualized Experiments, MyJove Corporation, , No. 147 ( 2019-05-06)
    Type of Medium: Online Resource
    ISSN: 1940-087X
    URL: Article
    DOI: 10.3791/59531
    Language: English
    Publisher: MyJove Corporation
    Publication Date: 2019
    detail.hit.zdb_id: 2259946-0
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