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Rotation Projects: <p >Potential rotation projects My lab primarily investigates Plasmodium falciparum malaria-induced dysregulation of EBV-specific T cell immunity and its role in the etiology of endemic Burkitt lymphoma (eBL), the most prevalent pediatric cancer in Equatorial Africa. Within the context of our ongoing studies of healthy Kenyan children with divergent malaria exposure histories (chronic/repeated infections in a holoendemic area versus low infection rates in a nearby highland, malaria hypoendemic area) and by examining children diagnosed with eBL we have established a repository of samples that can be used to address this question. <p >1. One avenue of exploration involves homeostatic cytokine regulation of memory T cells. IL-15 and/or IL-7 responsiveness of EBV-specific memory T cells may be impaired in children with chronic malaria exposure and in children with endemic Burkitt lymphoma (eBL). We would like to investigate IL-15Ra and IL-7Ra surface expression, and CFSE proliferation of EBV-specific T cells in response to cognate antigen with and without IL-15 or IL-7 stimulation and compared children with divergent malaria exposure histories and children diagnosed with eBL. T cell responsiveness to IL-15 and IL-7 can be measured by STAT5 phosphorylation and the specificity of this effect for EBV-specific T cells can be evaluated by comparing IL-15Ra and IL-7Ra expression and responsiveness on other lymphocyte subsets and CMV-specific T cells. <p >2. Another putative mechanism by which malaria may interfere with the development of immunologic memory and influence EBV-specific T cell immunity is through the Programmed death-1 (PD-1) pathway. PD-1 is an immune inhibitory molecule that negatively regulates activated immune cells upon interacting with its ligands, programmed death ligand-1 (PD-L1) and programmed death ligand-2 (PD-L2) resulting in down-regulation of immune responses. Previous studies in murine and primate viral and parasitic diseases have reported the up-r…
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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
first name: Karen
last name: Wiss
full name: Karen Wiss MD
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Person ID: 599
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Summary: Interests: Pediatric dermatology, epidermolysis bullosa, genodermatoses, midline developmental defects, childhood exanthems, medical education, pediatric laser
preferred title: Professor Emeritus

Bandini, Linda
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Sullivan-Bolyai, Susan
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Goldberg, Robert
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Belazarian, Leah
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Person ID: 785
person in primary position: Associate Professor
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Summary: Interests: Pediatric dermatology, psoriasis, genodermatoses, medical dermatology, inpatient dermatology
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Dvir, Yael
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McManus, David
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Morgan, Wynne
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Pediatric Genetics
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UMass Chan – Baystate Regional Campus
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Dermatology
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Boos, Stephen
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https://profiles.umassmed.edu/profile/16236519
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Lindenauer, Peter
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Copeland, Laurel
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ADJUNCT ASSOCIATE PROFESSOR
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Braverman, Paula
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Strauss, Kevin
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Population and Quantitative Health Sciences
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Minh, Hoang
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Schlaug, Gottfried
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Yonkers, Kimberly
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Garg, Arvin
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Broder-Fingert, Sarabeth
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Day, Philip
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Daly, Brian
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Lin, Honghuang
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Sorrentino, Renee
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Healthcare Delivery and Population Sciences at UMass Chan - Baystate
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Neurology at UMass Chan - Baystate
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Pediatrics at UMass Chan - Baystate
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Perepletchikova, Francheska
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Johnson-Agbakwu, Crista
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Sheldrick, Radley
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Driban, Jeffrey
first name: Jeffrey
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Featured Videos: https://profiles.umassmed.edu/profile/40402890
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Kelly, Lourah
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https://profiles.umassmed.edu/profile/36583234
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Anesthesiology at UMass Chan - Lahey
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Medicine at UMass Chan - Lahey
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https://profiles.umassmed.edu/profile/40402890
ProfilesRNS Plugin Searchable Data: Preventing Osteoarthritis After an ACL Injury
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Professor
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Su, Shaobing
first name: Shaobing
last name: Su
full name: Shaobing Su PhD, MEd
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Post Docs: Dr. Xihan Yang is a postdoctoral fellow at the Family Resilience and Child Development (FRCD) Lab. She received a PhD degree from the Department of Child Study and Human Development at Tufts University. Xihan's career goal is to conduct research to understand the intersectional effects of culture and neurodiversity to serve and protect minority child populations, especially underserved autistic children from immigrant families. During her postdoctoral training, Xihan will collaborate with Shaobing on an NIH R00 mixed-methods project focusing on parent-child separation and child mental health among low-income Chinese immigrant families. She will also support Shaobing’s mentoring practices for student research assistants at the lab.
Summary: The Family Resilience and Child Development (FRCD) lab, led by Dr. Shaobing Su, focuses on developmental research with vulnerable and underserved children affected by various forms of family separation, especially those related to parental migration and immigration. The lab's mission is to understand and address health disparities related to family separation in various contexts.
preferred title: Assistant Professor

Radiology at UMass Chan - Lahey
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Professor
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Health System Science
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Infectious Diseases
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Pulmonary Medicine
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Professor
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Associate Professor
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Assistant Professor
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General Pediatrics
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Ob/Gyn General
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Pediatric Research
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Chair and Professor
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Geissler, Kimberley
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Tan Chingfen Graduate School of Nursing
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Professor Emeritus
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Professor Emeritus
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McAlindon, Timothy
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Martinez, Fernando
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Endowed Chair Honorary Title: Joseph D. Early Chair in Biomedical Research
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Professor
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Professor Emeritus
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Krings, Timo
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Swanson, Jeffrey
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Assistant Professor
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Maron, Martin
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Maron, Barry
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Adjunct Professor
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Professor
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Christensen, Maxwell
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