This T32 Post-Doctoral training program has been funded by NIAID since July, 1994. The faculty mennbers are from three neighboring institutes: University of California, San Diego (UCSD), and the La Jolla Institute for Allergy and Immunology (LIAI), which are both housed on the UCSD campus, and The Scripps Research Institute (TSRI) which is next door to UCSD. The trainees will have opportunities to be exposed to a wide range of allergy research topics. In addition, the inter-institutional training program serves as a catalyst for promoting interactions and collaborations among researchers from different institutes. All faculty members have well established research programs;their research backgrounds are diverse and when taken together encomjDass allergy, immunology, genetics, biochemistry, cell biology, signal transduction, glycobiology, and molecular biology. Therefore, this training program represents an interdisciplinary approach. The trainees can be involved in the following research areas: 1) regulation of IgE production, including Th1/Th2 differentiation;2) biology of inflammatory cells, including mast cells and eosinophils;3) biology of T cells;4) cell receptors critically involved in allergic reactions;5) signal transduction;6) inflammatory mediators/cytokines;7) functions of epithelial cells;and 7) adhesion. The goals of the program are 1) to provide trainees with a basic understanding of pathogenesis of allergic diseases;and 2) to foster the development of trainee's investigative skills, in particular, applying molecular and cellular biological approaches to study mechanisms of diseases. The program is open to MD's and Ph.D.'s interested in disease-oriented problems and committed to a career in basic research in clinical sciences. The trainee's are expected to devote full time to research, and training will be supplemented by conferences, seminars, journal clubs and courses. It can be expected that trainees will develop a solid background in the pathogenesis of allergic diseases and molecular and cellular mechanisms of allergic inflammation and become qualified and confident in embarking upon their careers as independent investigators in allergy research. The broad expertise and experience the trainees acquire will prepare them for independent research in biomedicine.
The post-doctoral training of physician scientists and PhD's in mechanisms of allergic inflammation is important in providing trainees with the needed expertise to translate basic science advances to improvements in health care for patients with allergic disease by joining academia or biotechnology following their training.
|Das, Sudipta; Miller, Marina; Beppu, Andrew K et al. (2016) GSDMB induces an asthma phenotype characterized by increased airway responsiveness and remodeling without lung inflammation. Proc Natl Acad Sci U S A 113:13132-13137|
|Karta, Maya R; Broide, David H; Doherty, Taylor A (2016) Insights into Group 2 Innate Lymphoid Cells in Human Airway Disease. Curr Allergy Asthma Rep 16:8|
|Kim, Alexander S; Doherty, Taylor A; Karta, Maya R et al. (2016) Regulatory B cells and T follicular helper cells are reduced in allergic rhinitis. J Allergy Clin Immunol 138:1192-1195.e5|
|PiÃ±a, Francisco Javier; Fleming, Tinya; Pogliano, Kit et al. (2016) Reticulons Regulate the ER Inheritance Block during ER Stress. Dev Cell 37:279-88|
|Tse, Kevin; Chen, Lie; Tse, Mabel et al. (2015) Effect of catastrophic wildfires on asthmatic outcomes in obese children: breathing fire. Ann Allergy Asthma Immunol 114:308-311.e4|
|PiÃ±a, Francisco J; Niwa, Maho (2015) The ER Stress Surveillance (ERSU) pathway regulates daughter cell ER protein aggregate inheritance. Elife 4:|
|Doherty, Taylor A; Baum, Rachel; Newbury, Robert O et al. (2015) Group 2 innate lymphocytes (ILC2) are enriched in active eosinophilic esophagitis. J Allergy Clin Immunol 136:792-794.e3|
|Walford, Hannah H; Zuraw, Bruce L (2014) Current update on cellular and molecular mechanisms of hereditary angioedema. Ann Allergy Asthma Immunol 112:413-8|
|Tam, Arvin B; Koong, Albert C; Niwa, Maho (2014) Ire1 has distinct catalytic mechanisms for XBP1/HAC1 splicing and RIDD. Cell Rep 9:850-8|
|Yu, Jiujiu; Nagasu, Hajime; Murakami, Tomohiko et al. (2014) Inflammasome activation leads to Caspase-1-dependent mitochondrial damage and block of mitophagy. Proc Natl Acad Sci U S A 111:15514-9|
Showing the most recent 10 out of 42 publications