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Post Docs: A postdoc position is available to study in Dr. Ceol's lab.Click here to apply.
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Post Docs: Immediate opening! Two postdoctoral positions are available immediately to study cellular andmolecular mechanisms resulting in immunosuppression after alcohol use. Thefocus of this research is the role of monocytes and dendritic cells indecreased antigen-specific T cell activation after alcohol use.Intracellular signalling mechanisms resulting in decreased NF-kBactivation and inflammatory cytokine induction after acute alcoholconsumption are being investigated. Please contact Dr. Szabo for details.
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Endowed Chair Honorary Title: Lambi and Sarah Adams Chair in Genetic Research
Rotation Projects: Rotations: Targeting the IFN-?-chemokine axis for treatment of vitiligo: We are using our newly developed mouse model and human tissues from patients with vitiligo to identify the cytokines and chemokines that are expressed within the depigmenting skin and which skin cells produce them. We are using genetically modified mouse strains (knockouts, conditional knockouts, fluorescent reporter strains), and cytokine and chemokine neutralizing antibodies to identify the key proteins required for disease. This data will permit us to rationally develop and test new therapeutic agents. Understanding the proinflammatory signals generated by melanocytes under cellular stress. Melanocytes from vitiligo patients have intrinsic abnormalities, including cellular stress evidenced by increased production of reactive oxygen species (ROS) and activation of the unfolded protein response (UPR). The immune system has evolved to recognize this stress as damage-associated molecular patterns (DAMPs), which activate innate immunity. We are using human cells and tissues to determine how cellular stress, innate immunity, and adaptive immunity cooperate to initiate and perpetuate depigmentation in vitiligo. Developing a humanized mouse model of immune-skin interactions to serve as a pre-clinical bridge to clinical studies: We are developing a humanized mouse model of skin disease that consists of an immunodeficient mouse strain as a host for an autologous human skin graft and immune reconstitution in order to study mechanisms of inflammation in the skin, including allergic contact dermatitis, response to infection, tumor immunotherapy, and autoimmunity, all within a fully human environment. This model system will act as a pre-clinical bridge between mouse models and human clinical trials, providing an opportunity to test new treatments on human cells and tissues prior to initiating trials on patients. Tracking real-time autoreactive T cell migration and interactions within the skin: We are usin…
Rotation Projects: Rotations: Targeting the IFN-g-chemokine axis for treatment of vitiligo: We are using our newly developed mouse model and human tissues from patients with vitiligo to identify the cytokines and chemokines that are expressed within the depigmenting skin and which skin cells produce them. We are using genetically modified mouse strains (knockouts, conditional knockouts, fluorescent reporter strains), and cytokine and chemokine neutralizing antibodies to identify the key proteins required for disease. This data will permit us to rationally develop and test new therapeutic agents. Understanding the proinflammatory signals generated by melanocytes under cellular stress. Melanocytes from vitiligo patients have intrinsic abnormalities, including cellular stress evidenced by increased production of reactive oxygen species (ROS) and activation of the unfolded protein response (UPR). The immune system has evolved to recognize this stress as damage-associated molecular patterns (DAMPs), which activate innate immunity. We are using human cells and tissues to determine how cellular stress, innate immunity, and adaptive immunity cooperate to initiate and perpetuate depigmentation in vitiligo. Developing a humanized mouse model of immune-skin interactions to serve as a pre-clinical bridge to clinical studies: We are developing a humanized mouse model of skin disease that consists of an immunodeficient mouse strain as a host for an autologous human skin graft and immune reconstitution in order to study mechanisms of inflammation in the skin, including allergic contact dermatitis, response to infection, tumor immunotherapy, and autoimmunity, all within a fully human environment. This model system will act as a pre-clinical bridge between mouse models and human clinical trials, providing an opportunity to test new treatments on human cells and tissues prior to initiating trials on patients. Tracking autoreactive T cell interactions within the skin: We are using fluorescently tagged C…
Summary: Interests: Vitiligo, autoimmunity, immunology, translational research
preferred title: Adjunct Professor

Wiss, Karen
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Rotation Projects: Rotation projects are designed to expose students to the biology of adult stem cells, the mechanisms of tumorigenesis and to provide them with an appreciation for translational cancer research. These projects are focused on the major themes of the lab, which are: 1. Understanding the relative effects of oncogenic mutations on stem cells compared to the non-stem cell population from adult human skin. A key component of this project is to evaluate the Beta-catenin/Lef-1 signaling pathway on cultured epithelial stem cells and non-stem cells. 2. Studying the function of differently expressed genes in mediating stem cell behavior. The goal of this project is to understand the molecular mechanisms which control the critical properties of stem cell self-renewal, proliferation, adhesion and migration. 3. Identifying, isolating and characterizing “cancer stem cells” from human and mouse model tumors. Cancers are thought to possess a sub-population of slowly-cycling cancer stem cells which are responsible for tumor growth, recurrence and metastasis. The goal of this project is to begin to characterize these cells to help better target them therapeutically. The goal for all of these projects is to use the data obtained to help understand human tumorigenesis at the molecular, cellular and tissue levels, and be able to devise better treatments.
preferred title: Associate Professor

McManus, David
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Professor
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Professor
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Shin, Dong-Soo
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