October 9 - 12, 2012
Building 10 & Natcher Conference Center
- General Schedule of Events
- Opening Plenary Session
- Concurrent Symposia Sessions
- Poster Sessions
- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
- TSA Research Festival Exhibit Show
- Clinical Center Tours
- Research Festival Committees
- Past Research Festivals
Hematopoietic prostaglandin D synthase defines a subset of "super-effector" Th2 cells with enhanced function and an innate lymphoid program
| Friday, November 08, 2013 — Poster Session IV | |||
|---|---|---|---|
2:00 p.m. – 4:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NIAID |
IMMUNO-19 |
Authors
- A. Mitson-Salazar
- D. Wansley
- C. Prussin
Abstract
Th2 cells express IL-4, IL-5 and IL-13 and play a fundamental role in allergy and asthma pathogenesis. We have previously characterized two human Th2 subpopulations, IL-5- and IL-5+ Th2 cells, the latter being a highly differentiated subset of Th2 cells. Using microarray transcription profiling, we identified hematopoietic prostaglandin D synthase (hPGDS) as the most highly up-regulated gene expressed by IL-5+ Th2 cells. We thus used a monoclonal antibody to hPGDS to identify and characterize IL-5+ Th2 cells. hPGDS identified an IL-5bright Th2 subpopulation that was present in eosinophilic gastrointestinal disorder (EGID) subjects, but not healthy controls. The frequency of hPGDS+ Th2 cells was highly correlated to blood eosinophil count (r = 0.96). hPGDS+ Th2 cells expressed HLA-DR, PD-1, and TSLP-R, but not CD27 or IL-7R, consistent with highly differentiated effector cells. In response to activation with a variety of cytokines (IL-2, IL-25, IL-33, TSLP), hPGDS+ Th2 cells produced more IL-5 and IL-13 than did hPGDS- Th2. In this work we have characterized a novel subpopulation of "super-effector" Th2 cells that have enhanced effector function and are highly correlated to eosinophilic disease. These data strongly support a role for hPGDS+ Th2 cells in the pathogenesis of allergic inflammation.
