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    The Role of PD-1 and Its Ligands in Mercury(Hg)-induced Autoimmunity

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    Genre
    Thesis/Dissertation
    Date
    2009
    Author
    Piaggio, Eduardo
    Advisor
    Monestier, Marc
    Committee member
    Buttaro, Bettina A.
    Ganea, Doina
    Tsygankov, Alexander Y.
    Cohen, Philip L.
    Denny, Michael F.
    Department
    Microbiology and Immunology
    Subject
    Health Sciences, Immunology
    Autoimmunity
    Mercury
    Pd-1
    Permanent link to this record
    http://hdl.handle.net/20.500.12613/2155
    
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    DOI
    http://dx.doi.org/10.34944/dspace/2137
    Abstract
    The development of autoimmune diseases is frequently linked to exposure to environmental factors such as chemicals, drugs or infections. In the experimental model of metal-induced autoimmunity, administration of subtoxic doses of mercury (a common environmental pollutant) to genetically susceptible mice induces an autoimmune syndrome with rapid anti-nucleolar antibody production and immune system activation. Regulatory components of the innate immune system such as the costimulatory molecules PD-1, CTLA-4 and their ligands PD-L1, PD-L2, B7-1 and B7-2 can also modulate the autoimmune process. We examined the interplay among environmental chemicals and these costimulatory molecules in the regulation of autoimmunity. Additionally, we studied PD-1, CTLA-4 and its ligands in a tolerance model where pre-administration of a low dose of mercury in the steady state renders animals tolerant to metal-induced autoimmunity. Overall, PD-1/CTLA-4 blockade by blocking antibodies enhanced the manifestations of metal-induced autoimmunity. Although we expected that the blockade of both PD-1 ligands would mimic blocking the receptor, blocking the ligands resulted in the opposite effect when co-injected with mercury, reducing the manifestations of metal-induced autoimmunity. Individual PD-1 ligands differed in their ability to enhance the mercury treatment, with PD-L1 being the major regulator in the model. Likewise, we showed that PD-L1 is essential to keep the recall response to mercury at check. Our data suggest that these effects could be mediated by the modification of cytokine profiles, B cells and T cell subpopulations numbers.
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