The Biology and Pathology of Innate Immunity Mechanisms

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Leah Cook, Ph. Within bone, metastatic cancer cells highjack the normal couple process of bone remodeling, resulting in excess bone degradation and subsequent release of growth factors that promote tumor growth. Additionally, cancer cells progress and mediate bone turnover through molecular and cellular interactions with the surrounding bone stroma. My goal is to identify novel immunotherapeutic targets for treating and curing bone metastatic cancers.

The Biology and Pathology of Innate Immunity Mechanisms | Yona Keisari | Springer

Cook's research is also listed under Cancer Metastasis. Her laboratory has a long-standing interest in studying the pathogenesis and immune responses elicited by Staphylococcus aureus S. To this end, her laboratory has developed mouse models of biofilm infection associated with orthopedic implants and cranial bone flaps that accurately mimic the attributes of biofilm infections in humans. Her laboratory was the first to propose that S. This is achieved by the preferential recruitment of myeloid-derived suppressor cells MDSCs in addition to polarizing macrophage infiltrates towards an anti-inflammatory, pro-fibrotic phenotype.

Ongoing studies are to identify the mechanisms responsible for skewing the host innate immune response to an anti-inflammatory state following S. Her laboratory is utilizing high-throughput next-generation sequencing approaches RNA-Seq and Tn-Seq to elucidate critical molecules that promote biofilm development from both the host and bacterial perspectives.

Immune System: Diseases, Disorders & Function

The laboratory uses both human cells and mouse models to measure responses to inflammatory stimuli. In the Harris lab we study vitiligo, an autoimmune disease where cytotoxic T cells migrate into the skin and destroy melanocytes, the pigment-producing cells. There is evidence that vitiligo begins with induced cellular stress within melanocytes, and that this stress activates innate inflammatory pathways.

We are studying this process, and how innate inflammation translates into T cell-mediated autoimmunity. My lab studies the development of the innate immune response to DNA and RNA viruses, particularly in the lung and brain.

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Our focus is on TLRs and cytosolic innate immune signaling receptors and how these sensors promote the development of inflammation and adaptive immunity and influence disease outcome. Model systems that we utilize include bacterial infections with Yersinia pestis the causative agent of plague , Salmonella, other pathogens and also non-infectious inflammation.

Furthermore, we are interested in vaccines and mechanisms for adjuvant action. Research in the Levitz laboratory is focused on the mechanisms by which the immune system controls specific fungal pathogens and the strategies that fungi utilize to circumvent host defenses. Particular areas of interest include how fungal glycosylation influences immune responses, inflammasome stimulation by chitosan, the mechanisms by which plasmacytoid dendritic cells mediate protection against Aspergillus fumigatus and the development of vaccines against Cryptococcus neoformans and other pathogens.

Research in the Pukkila-Worley lab is focused on identifying innate immune pathways in the host and virulence-related signaling mechanisms in the pathogen that can be exploited to develop novel anti-infective small molecules. Towards this end, we are defining evolutionarily conserved means of innate immune activation using bacterial and fungal pathogenesis assays in the microscopic nematode Caenorhabditis elegans.

My group studies how bacteria specifically, the bacteria that cause gonorrhea and meningitis escape killing by the complement system.

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Knowledge of such immune evasion mechanisms are being translated to develop novel vaccines and therapies. My research identifies unique bacterial determinants that serve as suitable vaccine candidates to protect against infection in humans. Usually these determinants activate complement C that combats invading bacteria and also facilitates and amplifies the development of adaptive immune responses. Under certain conditions, C-regulators are hijacked by microorganisms and down-regulate the activation and binding of active C components and divert organisms to non-professional phagocytes epithelial cells where they can gain sanctuary.

In a separate line of inquiry, my laboratory also develops peptide mimics immunologic counterparts [surrogates] of suitable carbohydrate vaccine candidates to circumvent the disadvantages of carbohydrate-based vaccines.

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These simple peptides can then be used as vaccines to elicit protective immune responses. The major focus of the Rothstein lab is to understand the role of innate immune sensors in the activation of autoreactive B cells and T cells in models of systemic autoimmunity, autoinflammation, and fibrosi. We use particular interested in responses to nucleic acid associated autoantigens and the interplay between cytosolic and endosomal sensors in the regulation of relevant effector populations.

Using Drosophila melanogaster as model system, the Silverman lab focuses on the molecular mechanisms and physiological systems that control innate immunity, especially NF-kB signaling.