Research in the Nicola Heller Lab focuses on the immunobiology of macrophages. Our team explores how these cells impact diseases with an inflammatory element, such as cancer, cardiovascular disease and obesity. Using a variety of techniques, including molecular and cellular biology, biochemistry, mouse models and more, we study the role of IL-4/IL-13 signaling in asthma and allergic disease, as well as the role of alternatively activated macrophages (AAM) in the pathogenesis of allergic inflammation. Currently, we are researching the links between asthma and obesity, with a focus on the roles of gender and race.

The research activities of the Neuroimmunopathology Laboratory focus on studies of immunological and molecular mechanisms involved in the pathogenesis of neurological disorders. Our main areas of research include studies of neurological complications of HIV infection and AIDS, multiple sclerosis, transverse myelitis, autism and epilepsy. We seek to explore and identify immunopathological mechanisms associated with neurological disease that may be the target of potential therapeutic interventions. The laboratory collaborates with other researchers and laboratories at Johns Hopkins and other institutions in projects related with studies of the interaction between the immune and central nervous systems in pathological processes leading to neurological dysfunction.

David Hackam’s laboratory focuses on necrotizing enterocolitis (NEC), a devastating disease of premature infants and the leading cause of death and disability from gastrointestinal disease in newborns. The disease strikes acutely and without warning, causing sudden death of the small and large intestines. In severe cases, tiny patients with the disease are either dying or dead from overwhelming sepsis within 24 hours. Surgical treatment to remove most of the affected gut results in lifelong short gut (short bowel) syndrome. The Hackam Lab has identified a critical role for the innate immune receptor toll-like receptor 4 (TLR4) in the pathogenesis of necrotizing enterocolitis. The lab has shown that TLR4 regulates the development of the disease by tipping the balance between injury and repair in the stressed intestine of the premature infant. Developing an Artificial Intestine A key goal is to create, in the laboratory, new intestines made from patients’ own cells, which can then be implanted into the patient to restore normal digestive function. This innovative design could transform child development and quality of life in necrotizing enterocolitis survivors without the risks of conventional donor transplant.

Dr. Rabb’s lab is involved in translational research aimed at understanding the molecular pathogenesis of kidney ischemia/reperfusion injury. The lab is interested in the development of novel treatments for kidney IRI.

Dr. Atta and his research team explore the epidemiological and clinical interventions of a variety of kidney diseases. Our goal is not only to advance the understanding of many kidney diseases but also to capitalize on novel discoveries of basic science to treat a wide range of rare and common kidney disorders.

• Multi-international observational study of a rare form of amyloid (LECT2 amyloid) to understand its natural history with the ultimate interest of treating this condition.
• Our group has launched a project investigating the impact of COVID19 on the kidney to identify risk factors influencing outcome across different clinical phenotypes
• In collaboration with the Division of Infectious Diseases and the School of Public Health, our research has focused on the epidemiology of HIV and kidney disease. We also study clinical markers and contributing factors in the progression of kidney disease, and the association between kidney disease and heart disease.
• Our research group is participating in a multicenter consortium serving as a clinical core site to study the pathogenesis of HIV-associated kidney disease by providing well-characterized clinical specimens and corresponding clinical and laboratory data.

Our laboratory conducts basic and translational research aimed at better understanding the pathogenesis of multiple sclerosis (MS) and the role of the immune system in CNS disease, particularly the processes that drive progressive disability such as neurodegeneration and remyelination failure. We currently have three parallel research programs: 1. Metabolism as a modulator of MS: We are studying how basic metabolic pathways regulate the immune system and how these pathways might be exploited to protect neurons and myelin-forming oligodendrocytes from injury. 2. Identifying pathways by which nitric oxide (NO) and other free radicals cause neuronal and axonal damage. Our lab is identifying specific signaling pathways initiated by NO and other free radicals that can be targeted by drugs to produce neuroprotection. 3. Modulating the innate immune system in MS: In collaboration with others at Johns Hopkins, we are studying ways to enhance the reparative functions of microglia while preventing maladaptive responses. This work has identified bryostatin-1 as a potential drug that may be re-purposed for this task.

The Michael B. Streiff Lab conducts clinical and laboratory research of thrombophilia associated with malignancy. We are interested in the application of novel coagulation assays to explore the pathogenesis of thrombosis and the development of strategies to enhance the clinical management of anti-thrombotic agents.

Research in the Thomas Grader-Beck Lab aims to understand the pathogenesis of systemic autoimmune diseases—particularly systemic lupus erythematosus (SLE) and Sjögren’s syndrome—by taking a translational approach. Autoantibodies (antibodies that target self-molecules) are believed to contribute significantly to the disease process. We are studying mechanisms that may make self-structures immunogenic. We theorize that certain post-translational antigen modifications, which can occur in infections or malignant transformation, result in the expression of neoepitopes that spread autoimmunity in the proper setting. The team has combined studies that employ a number of mouse strains, certain gene-deficient mice and human biological specimens.

The goals of the Translational neurobiology Laboratory are to understand the pathogenesis and cell death pathways in neurodegenerative disorders to reveal potential therapeutic targets for pharmaceutical intervention; to investigate endogenous survival pathways and try to induce these pathways to restore full function or replace lost neurons; and to identify biomarkers to mark disease function or replace lost neurons; and to identify biomarkers to mark disease progression and evaluate therapeutics. Our research projects focus on models of Huntington's disease and Parkinson's disease. We use a combination of cell biology and transgenic animal models of these diseases.

The Stivers Lab is broadly interested in the biology of the RNA base uracil when it is present in DNA. Our work involves structural and biophysical studies of uracil recognition by DNA repair enzymes, the central role of uracil in adapative and innate immunity, and the function of uracil in antifolate and fluoropyrimidine chemotherapy. We use a wide breadth of structural, chemical, genetic and biophysical approaches that provide a fundamental understanding of molecular function. Our long-range goal is to use this understanding to design novel small molecules that alter biological pathways within a cellular environment. One approach we are developing is the high-throughput synthesis and screening of small molecule libraries directed at important targets in cancer and HIV-1 pathogenesis.