University of Rochester School of Medicine
Pathways of Human Disease Student at computer in research lab office

Research Opportunities by Human Disease:

Cancer | Cardiovascular Disease | Endocrine Disorders |
Genetic Diseases | Immunology and Hematology |
Musculoskeletal Diseases | Neurologic Disorders


Immunology and Hematology

Elucidation of the various cell types in blood (neutrophils, macrophages, T-cells, B-cells) and their specific role in host defense has transformed medicine and our ability to treat human disease. When these cells work together appropriately the host is able to fight off infection and clear cancerous cells. However, when these cells and their products (antibodies, cytokines) become dysregulated serious autoimmune pathology can occur (rheumatoid arthritis, lupus, diabetes). Based on this knowledge, there are now FDA approved biologic therapies that target specific cells and their products to ameliorate autoimmune disease and cancer.

Current research in this area is focused on further understanding the interaction of these different cells with each other and in specific tissues (liver, pancreas, brain) to identify the genes the mediate this regulation. Exciting opportunities are available in several labs within our program to study the molecular genetics and pathophysiology of autoimmunity, microbial pathogenesis and cancer using genetically engineered animal models and novel therapeutic interventions.

Faculty investigating diseases of the immune system and blood:

Laura Calvi
Lisa Demeter
Philip Fay
Alan Friedman
Laurie Milner
James Palis

Robert Pierce

Ignacio Sanz

Edward Schwarz
Peter Sims
Harold Smith
Therese Wiedmer
Terry Wright
Fay Young


 

 

Staining of antibodies in SLE

Autroreactive B-cells, identified with the anti-idiotypic antibody 9G4 (in green) do not form germinal centers (GC, stained blue by anti-CD38 antibodies) in healthy subjects (top photograph). Instead, they accumulate in the follicular mantle (painted red by anti-IgD antibodies). In contrast, patients with SLE (systemic lupus) cannot censor autoreactive B-cells from forming productive GC. These studies represent the first definition of a defective B-cell tolerance checkpoint in human SLE.

Images courtesy of Dr. Ignacio Sanz.

 

 


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Last updated: 07/02/2007 10:23 AM

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