Novel innate lymphocyte pathways controlling mucosal immunity

The National Institute of Allergy and Infectious Diseases awarded a Cooperative Agreement totaling $581,915 to Weill Medical College of Cornell University on July 21, 2026, to investigate novel innate lymphocyte pathways controlling mucosal immunity under the Allergy and Infectious Diseases Research program (CFDA 93.855).

The recipient will identify and characterize two previously unappreciated cell-intrinsic pathways that control innate lymphocyte biology and mucosal immune responses, with particular focus on type-2 and type-17 mucosal immunity. The work will define how these pathways shape mucosal inflammation in human subjects with mucosal inflammatory conditions and test innovative pre-clinical therapeutic approaches. Results are expected to generate mechanistic insights supporting preventative, therapeutic, or curative treatment strategies for infection and inflammation of the airway and intestine.

Performance of work occurs at Weill Medical College's New York, New York location (10065). The period of performance runs from July 21, 2026, through May 30, 2031.

Abstract

Mucosal immunity is necessary for human health by acting at barrier surfaces, including the airway or intestine, to promote tissue physiology, enforce tolerance, aid in reparative processes, and protect from infection. However, uncontrolled mucosal immunity is a driver of chronic inflammatory disorders, such as inflammatory bowel disease (IBD) and allergy. The fundamental focus of this application to join the mucosal immunology studies team is to harness new approaches and uncover novel biology on innate lymphocytes that will permit development of innovative strategies to enhance protective, and limit pathologic, mucosal immunity. Specifically, our prior proposal builds on a strong rigor of prior research detailing how innate lymphocytes are essential components of both type-2 and type-17 mucosal immunity. In new preliminary data, we developed new approaches to study innate lymphocytes, which identified two previously unappreciated, surprising, and complementary cell-intrinsic pathways controlling cellular biology and mucosal immune responses. Further, we find that these cellular pathways are dysregulated in the context of humans with mucosal inflammation. To address this further, we propose two specific aims, which will define two novel pathways that shape innate lymphocyte biology and dramatically control mucosal immunity and inflammation, as well as test innovative pre-clinical therapies. We expect our mechanistic results will provoke new opportunities for preventative, therapeutic or curative treatment strategies in infection & inflammation of the airway and intestine.