Origin and programming of fetal group 1 lymphoid cells
Active Project Grant Awarded Last action
- Award ID
- F30AI203419
- Recipient
-
Cornell University UEI G56PUALJ3KT5
- Awarding agency
-
National Institute of Allergy and Infectious Diseases
National Institutes of Health, Department of Health and Human Services
- Obligated
- $44,452
Award facts
- Assistance listing
- 93.855 Allergy and Infectious Diseases Research
- Completion date 0% complete
- Place of performance
- New York, USA
Award details come from USAspending.gov.
Description
- Abstract
- Over the last two decades there has been a growing appreciation for the unique contributions of fetal hematopoiesis to the immune system. We now know that early fetal progenitors are capable of producing B cells, T cells, and macrophages that are functionally distinct from their hematopoietic stem cell (HSC)-derived counterparts. By contrast, our understanding of natural killer (NK) and type 1 innate lymphoid cell (ILC1) development is much more limited. This is a crucial knowledge GAP, especially considering the important role that NK and ILC1S-collectively termed group 1 innate lymphoid cells (ILC)-play in controlling infection and cancer. There is some evidence that fetal-derived group 1 ilcs possess unique functions compared to their counterparts generated in adulthood. However, the specific embryonic progenitors that produce fetal-derived group 1 ilcs and the molecular regulators that underlie their development have yet to be clearly defined. Interestingly, my preliminary data suggests that fetal-derived group 1 ilcs arise from hemogenic endothelial cells in the yolk SAC prior to the emergence of hscs. Moreover, I found that forced expression of LIN28B enables adult hscs to give rise to group 1 ilcs that behave similarly to those found in neonates. Based on these data, I hypothesize that LIN28B expression in HSC-independent progenitors promotes the development of fetal-derived group 1 ilcs. In aim 1, I will use in vitro artificial organoids and in vivo approaches to map the development of group 1 ilcs from various embryonic progenitors. In aim 2, I will use LIN28B knockout and transgenic mouse models to determine the necessity and sufficiency of LIN28B in programming fetal group 1 ILC functions. Throughout this project, I will receive integrated training from an innovative team of scientific and clinical mentors that will position me to launch a successful career in translational immunology research. Altogether, my findings will advance our understanding of how fetal origins shape early life immunity and provide novel genetic targets that tailor group 1 ILC functions to better fight off disease.
Quick answers
Who received award F30AI203419?
F30AI203419 was awarded to Cornell University by National Institute of Allergy and Infectious Diseases (National Institutes of Health) on February 6, 2027.
How much is award F30AI203419 worth?
$44,452 has been obligated on F30AI203419.
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