Cellular therapy of Blood Diseases
Can modification of either autologous or allogeneic immune cells allow effective treatment of blood diseases and infection with acceptable rates of toxicity?
Can modification of either autologous or allogeneic immune cells allow effective treatment of blood diseases and infection with acceptable rates of toxicity?
What triggers decompensation of cellular and molecular pathways during exacerbations of chronic lung diseases?
How can the use of CAR T-cell and checkpoint blockade strategies be optimized in order to cure hematologic diseases?
What are the molecular and cellular responses in the lung that occur after environmental stimuli that predict homeostatic resilience or transition to disease, disorder, or aging?
How do gene mutations in endoglin and alk 1 create arteriovenous malformations leading to disease. Alk 1 and endoglin are receptors in TGFB/BMP family signaling. TGFB/BMP have roles in vascular development, remodeling and maintenance in vascular integrity. Understanding the downstream effect will lead to advancements in reducing genetic diseases such as HHT as well as vascular malformations in general
Goal 3: Advance Translational Research
As the current chair of the Research and Training Division, I would like to convey that the AAAAI membership would like the NHLBI to consider the following in the development of its strategic plan:
What are the molecular and cellular responses in the lung that occur after environmental stimuli (including allergens) that predict homeostatic resilience or transition to atopic diseases?
Goal 3: Advance Translational Research
NHLBI might consider creating incentives for the development of core labs and national facilities to promote development of animal and cellular model systems that mimic lung injury, repair, and regeneration.