Abstract
Tregs play important roles in maintaining immune homeostasis, and thus, therapies based on Treg are promising candidates for the treatment for a variety of immune-mediated disorders. These therapies, however, face the significant challenge of obtaining adequate numbers of Tregs from peripheral blood that maintains suppressive function following extensive expansion. Inducing Tregs from non-Tregs offers a viable alternative. Different methods to induce Tregs have been proposed and involve mainly treating cells with TGF-β-iTreg. However, use of TGFβalone is not sufficient to induce stable Tregs. ATRA or rapa has been shown to synergize with TGF-βto induce stable Tregs. Whereas TGF-βplus RA-iTregs have been well-de-scribed in the literature, the phenotype, function, and migratory characteristics of TGF-βplus rapa-iTreg have yet to be elucidated. Herein, we describe the phenotype and function of mouse rapa-iTreg and reveal that these cells differ in their in vivo homing capacity when compared with mouse RA-iTreg and mouse TGF-βiTreg. This difference in migratory activity significantly affects the therapeutic capacity of each subset in a mouse model of colitis. We also describe the characteristics of iTreg generated in the presence of TGF-β, RA, and rapa.
Original language | English (US) |
---|---|
Pages (from-to) | 981-989 |
Number of pages | 9 |
Journal | Journal of Leukocyte Biology |
Volume | 94 |
Issue number | 5 |
DOIs | |
State | Published - Nov 2013 |
Keywords
- Adoptive cell
- Chemokines
- Inflammatory bowel disease
- Live-animal imaging
- Therapy
- Treg migration
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Cell Biology