| First Author | Jhunjhunwala S | Year | 2013 |
| Journal | J Leukoc Biol | Volume | 94 |
| Issue | 5 | Pages | 981-9 |
| PubMed ID | 23898044 | Mgi Jnum | J:209554 |
| Mgi Id | MGI:5568063 | Doi | 10.1189/jlb.0312167 |
| Citation | Jhunjhunwala S, et al. (2013) All-trans retinoic acid and rapamycin synergize with transforming growth factor-beta1 to induce regulatory T cells but confer different migratory capacities. J Leukoc Biol 94(5):981-9 |
| abstractText | 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-beta-iTreg. However, use of TGF-beta alone is not sufficient to induce stable Tregs. ATRA or rapa has been shown to synergize with TGF-beta to induce stable Tregs. Whereas TGF-beta plus RA-iTregs have been well-described in the literature, the phenotype, function, and migratory characteristics of TGF-beta plus 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-beta-iTreg. 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-beta, RA, and rapa. |
