The immunologic determinants of chronic cavitary TB versus TB latency
Event details
| Date | 20.04.2012 |
| Hour | 11:00 › 12:00 |
| Speaker | Gilla Kaplan, Public Health Research Institute Center, UMDNJ - New Jersey Medical School, Newark, USA |
| Location | |
| Category | Conferences - Seminars |
Research Summary
Gilla Kaplan, Ph.D., Professor of Medicine in the Laboratory of Mycobacterial Immunity and Pathogenesis at the Public Health Research Institute Center of the University of Medicine and Dentistry of New Jersey. Dr. Kaplan’s expertise encompasses studies of human disease and animal models to better understand host immune responses and the role of cytokine production in the pathogenesis of microbial infections. For the past 30 years, Dr. Kaplan has been studying the role of macrophage activation in the host response, initially to tumors and later to mycobacterial infections. She and her colleagues have studied immune responses to intradermal administration of recombinant interferon gamma (rIFN-Gamma), interleukin 2 (rIL2) and macrophage colony stimulating factor (rGM-CSF) in persons with lepromatous leprosy; examined T cell responsiveness and suppression in leprosy; defined immune activation and gene expression in patients with tuberculosis (TB) following treatment with rIL-2; and characterized interactions between M. tuberculosis and HIV or M. leprae and HIV in co-infected patients. More recently, Dr. Kaplan and her group determined that the production of macrophage proinflammatory cytokines are differentially induced following infection with different clinical isolates of M. tuberculosis, leading to different extents of disease progression and clinical outcome. Dr. Kaplan and her team have shown that thalidomide treatment modifies TNF-Alpha and IL-12 production and can improve outcome in humans with lepromatous leprosy, TB or HIV infection, in animal models of inhalational TB (in mice) and TB meningitis (in rabbits), and in vitroin M.tuberculosis-infected human monocytes. Dr. Kaplan and her team have since developed two classes of novel, synthetic analogues of thalidomide that reduce TNF-Alpha production by 50,000 times more than the parent drug, thalidomide, and with fewer deleterious side effects. Co-treatment with these analogues, in combination with antibiotics, is significantly more efficient in reducing TNF-Alpha production and improving survival of rabbits with experimental TB meningitis than antibiotic treatment alone. The immunomodulatory drugs are being further tested as adjunctive therapy to antibiotic treatment in mice and rabbits with pulmonary TB to reduce tissue injury and improve response to treatment.
Gilla Kaplan, Ph.D., Professor of Medicine in the Laboratory of Mycobacterial Immunity and Pathogenesis at the Public Health Research Institute Center of the University of Medicine and Dentistry of New Jersey. Dr. Kaplan’s expertise encompasses studies of human disease and animal models to better understand host immune responses and the role of cytokine production in the pathogenesis of microbial infections. For the past 30 years, Dr. Kaplan has been studying the role of macrophage activation in the host response, initially to tumors and later to mycobacterial infections. She and her colleagues have studied immune responses to intradermal administration of recombinant interferon gamma (rIFN-Gamma), interleukin 2 (rIL2) and macrophage colony stimulating factor (rGM-CSF) in persons with lepromatous leprosy; examined T cell responsiveness and suppression in leprosy; defined immune activation and gene expression in patients with tuberculosis (TB) following treatment with rIL-2; and characterized interactions between M. tuberculosis and HIV or M. leprae and HIV in co-infected patients. More recently, Dr. Kaplan and her group determined that the production of macrophage proinflammatory cytokines are differentially induced following infection with different clinical isolates of M. tuberculosis, leading to different extents of disease progression and clinical outcome. Dr. Kaplan and her team have shown that thalidomide treatment modifies TNF-Alpha and IL-12 production and can improve outcome in humans with lepromatous leprosy, TB or HIV infection, in animal models of inhalational TB (in mice) and TB meningitis (in rabbits), and in vitroin M.tuberculosis-infected human monocytes. Dr. Kaplan and her team have since developed two classes of novel, synthetic analogues of thalidomide that reduce TNF-Alpha production by 50,000 times more than the parent drug, thalidomide, and with fewer deleterious side effects. Co-treatment with these analogues, in combination with antibiotics, is significantly more efficient in reducing TNF-Alpha production and improving survival of rabbits with experimental TB meningitis than antibiotic treatment alone. The immunomodulatory drugs are being further tested as adjunctive therapy to antibiotic treatment in mice and rabbits with pulmonary TB to reduce tissue injury and improve response to treatment.
Practical information
- Informed public
- Free
Organizer
- The Global Health Institute, Prof. Stewart Cole