Immune Regulation

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The Experts below are selected from a list of 145938 Experts worldwide ranked by ideXlab platform

Andre Veillette - One of the best experts on this subject based on the ideXlab platform.

Randolph J Noelle - One of the best experts on this subject based on the ideXlab platform.

  • b7 family checkpoint regulators in Immune Regulation and disease
    Trends in Immunology, 2013
    Co-Authors: Sabrina Ceeraz, Randolph J Noelle, Elizabeth Nowak
    Abstract:

    Fine-tuning the Immune response and maintaining tolerance to self-antigens involves a complex network of co-stimulatory and co-inhibitory molecules. The recent FDA approval of ipilimumab, a monoclonal antibody blocking cytotoxic T lymphocyte antigen (CTLA)-4, demonstrates the impact of checkpoint regulators in disease. This is reinforced by ongoing clinical trials targeting not only CTLA-4, but also the programmed death (PD)-1 and B7-H4 pathways in various disease states. Recently, two new B7 family inhibitory ligands, V-domain Ig suppressor of T cell activation (VISTA) and B7-H6 were identified. Here, we review recent understanding of B7 family members and their concerted Regulation of the Immune response to either self or foreign pathogens. We also discuss clinical developments in targeting these pathways in different disease settings, and introduce VISTA as a putative therapeutic target.

  • Immune Regulation by cd40 and its ligand gp39
    Annual Review of Immunology, 1996
    Co-Authors: Teresa M Foy, Alejandro Aruffo, Jurgen Bajorath, Janet E Buhlmann, Randolph J Noelle
    Abstract:

    ▪ Abstract Over the past three years, CD40 and its ligand (gp39, CD40L, TBAM) have been shown to be essential for humoral Immune responses to thymus-dependent antigens. However, as the tissue distribution widens for those cells that express CD40 and gp39, we can now show that this ligand-receptor pair also plays an important role in the selection of self-reactive T cells in the thymus (central tolerance) and the Regulation of tolerance in mature T cells (peripheral tolerance). Advances in our understanding of the molecular basis for CD40 biology is based in two areas of research. First, a major breakthrough in our understanding of how CD40 transduces biological events centers on the identification of a novel protein that binds to the cytoplasmic tail of CD40 and may act as a signal transducing molecule. Secondly, advances in molecular modeling and mutagenesis of this ligand-receptor pair have helped to identify the critical receptor/ligand contacts in the gp39/CD40 complex. Advances in each of these areas...

  • Immune Regulation by cd40 and its ligand gp39
    Annual Review of Immunology, 1996
    Co-Authors: Teresa M Foy, Alejandro Aruffo, Jurgen Bajorath, Janet E Buhlmann, Randolph J Noelle
    Abstract:

    Over the past three years, CD40 and its ligand (gp39, CD40L, TBAM) have been shown to be essential for humoral Immune responses to thymus-dependent antigens. However, as the tissue distribution widens for those cells that express CD40 and gp39, we can now show that this ligand-receptor pair also plays an important role in the selection of self-reactive T cells in the thymus (central tolerance) and the Regulation of tolerance in mature T cells (peripheral tolerance). Advances in our understanding of the molecular basis for CD40 biology is based in two areas of research. First, a major breakthrough in our understanding of how CD40 transduces biological events centers on the identification of a novel protein that binds to the cytoplasmic tail of CD40 and may act as a signal transducing molecule. Secondly, advances in molecular modeling and mutagenesis of this ligand-receptor pair have helped to identify the critical receptor/ligand contacts in the gp39/CD40 complex. Advances in each of these areas are discussed.

Rajiv Khanna - One of the best experts on this subject based on the ideXlab platform.

  • bk polyomavirus clinical aspects Immune Regulation and emerging therapies
    Clinical Microbiology Reviews, 2017
    Co-Authors: George R Ambalathingal, Ross S Francis, Mark J Smyth, Corey Smith, Rajiv Khanna
    Abstract:

    BK polyomavirus (BKV) causes frequent infections during childhood and establishes persistent infections within renal tubular cells and the uroepithelium, with minimal clinical implications. However, reactivation of BKV in immunocompromised individuals following renal or hematopoietic stem cell transplantation may cause serious complications, including BKV-associated nephropathy (BKVAN), ureteric stenosis, or hemorrhagic cystitis. Implementation of more potent immunosuppression and increased posttransplant surveillance has resulted in a higher incidence of BKVAN. Antiviral immunity plays a crucial role in controlling BKV replication, and our increasing knowledge about host-virus interactions has led to the development of improved diagnostic tools and clinical management strategies. Currently, there are no effective antiviral agents for BKV infection, and the mainstay of managing reactivation is reduction of immunosuppression. Development of Immune-based therapies to combat BKV may provide new and exciting opportunities for the successful treatment of BKV-associated complications.

  • human cytomegalovirus clinical aspects Immune Regulation and emerging treatments
    Lancet Infectious Diseases, 2004
    Co-Authors: Maher K Gandhi, Rajiv Khanna
    Abstract:

    After initial infection, human cytomegalovirus remains in a persistent state with the host. Immunity against the virus controls replication, although intermitent viral shedding can still take place in the seropositive immunocompetent person. Replication of cytomegalovirus in the absence of an effective Immune response is central to the pathogenesis of disease. Therefore, complications are primarily seen in individuals whose Immune system is immature, or is suppressed by drug treatment or coinfection with other pathogens. Although our increasing knowledge of the host-virus relationship has lead to the development of new pharmacological strategies for cytomegalovirus-associated infections, these strategies all have limitations-eg, drug toxicities, development of resistance, poor oral bioavailability, and low potency. Immune-based therapies to complement pharmacological strategies for the successful treatment of virus-associated complications should be prospectively investigated.

Shokrollah Elahi - One of the best experts on this subject based on the ideXlab platform.

  • human leukocyte antigen hla and Immune Regulation how do classical and non classical hla alleles modulate Immune response to human immunodeficiency virus and hepatitis c virus infections
    Frontiers in Immunology, 2017
    Co-Authors: Nicole Crux, Shokrollah Elahi
    Abstract:

    The genetic factors associated with susceptibility or resistance to viral infections are likely to involve a sophisticated array of Immune-response. These genetic elements may modulate other biological factors that account for significant influence on the gene expression and/or protein function in the host. Among them, the role of the Major Histocompatibility Complex (MHC) in viral pathogenesis in particular HIV and HCV, is very well documented. We recently added a novel insight into the field by identifying the molecular mechanism associated with the protective role of HLA-B27/B57 CD8+ T cells in the context of HIV-1 infection and why these alleles act as a double-edged sword protecting against viral infections but predisposing the host to autoImmune diseases. The focus of this review will be reexamining the role of classical and non-classical HLA-alleles including class Ia (HLA-A, -B, -C), class Ib (HLA-E, -F, -G, -H) and class II (HLA-DR, -DQ, -DM, and -DP) in Immune Regulation and viral pathogenesis (e.g. HIV and HCV). To our knowledge this is the very first review of its kind to comprehensively analyze the role of these molecules in Immune Regulation associated with chronic viral infections.

  • Human Leukocyte Antigen (HLA) and Immune Regulation: How Do Classical and Non-Classical HLA Alleles Modulate Immune Response to Human Immunodeficiency Virus and Hepatitis C Virus Infections?
    Frontiers Media S.A., 2017
    Co-Authors: Nicole Crux, Shokrollah Elahi
    Abstract:

    The genetic factors associated with susceptibility or resistance to viral infections are likely to involve a sophisticated array of Immune response. These genetic elements may modulate other biological factors that account for significant influence on the gene expression and/or protein function in the host. Among them, the role of the major histocompatibility complex in viral pathogenesis in particular human immunodeficiency virus (HIV) and hepatitis C virus (HCV), is very well documented. We, recently, added a novel insight into the field by identifying the molecular mechanism associated with the protective role of human leukocyte antigen (HLA)-B27/B57 CD8+ T cells in the context of HIV-1 infection and why these alleles act as a double-edged sword protecting against viral infections but predisposing the host to autoImmune diseases. The focus of this review will be reexamining the role of classical and non-classical HLA alleles, including class Ia (HLA-A, -B, -C), class Ib (HLA-E, -F, -G, -H), and class II (HLA-DR, -DQ, -DM, and -DP) in Immune Regulation and viral pathogenesis (e.g., HIV and HCV). To our knowledge, this is the very first review of its kind to comprehensively analyze the role of these molecules in Immune Regulation associated with chronic viral infections

Fiona Powrie - One of the best experts on this subject based on the ideXlab platform.

  • dendritic cells in intestinal Immune Regulation
    Nature Reviews Immunology, 2008
    Co-Authors: Janine L Coombes, Fiona Powrie
    Abstract:

    A delicate balance between tolerance to commensal bacteria and immunity to pathogens occurs in the intestine. Intestinal dendritic cells have a central role in maintaining this balance and, as described here, some of the molecular pathways involved have recently been resolved.

  • essential role for cd103 in the t cell mediated Regulation of experimental colitis
    Journal of Experimental Medicine, 2005
    Co-Authors: Oliver Annacker, Janine L Coombes, Vivianne Malmstrom, Holm H Uhlig, Tim Bourne, Bengt Johanssonlindbom, William W Agace, Christina M Parker, Fiona Powrie
    Abstract:

    The integrin CD103 is highly expressed at mucosal sites, but its role in mucosal Immune Regulation remains poorly understood. We have analyzed the functional role of CD103 in intestinal Immune Regulation using the T cell transfer model of colitis. Our results show no mandatory role for CD103 expression on T cells for either the development or CD4(+)CD25(+) regulatory T (T reg) cell-mediated control of colitis. However, wild-type CD4(+)CD25(+) T cells were unable to prevent colitis in Immune-deficient recipients lacking CD103, demonstrating a nonredundant functional role for CD103 on host cells in T reg cell-mediated intestinal Immune Regulation. Non-T cell expression of CD103 is restricted primarily to CD11c(high) MHC class IIhigh dendritic cells (DCs). This DC population is present at a high frequency in the gut-associated lymphoid tissue and appears to mediate a distinct functional role. Thus, CD103(+) DCs, but not their CD103(-) counterparts, promoted expression of the gut-homing receptor CCR9 on T cells. Conversely, CD103(-) DCs promoted the differentiation of IFN-gamma-producing T cells. Collectively, these data suggest that CD103(+) and CD103(+) DCs represent functionally distinct subsets and that CD103 expression on DCs influences the balance between effector and regulatory T cell activity in the intestine.