| First Author | Griseri T | Year | 2010 |
| Journal | J Exp Med | Volume | 207 |
| Issue | 4 | Pages | 699-709 |
| PubMed ID | 20368580 | Mgi Jnum | J:161661 |
| Mgi Id | MGI:4460839 | Doi | 10.1084/jem.20091618 |
| Citation | Griseri T, et al. (2010) OX40 is required for regulatory T cell-mediated control of colitis. J Exp Med 207(4):699-709 |
| abstractText | The immune response in the gastrointestinal tract is a tightly controlled balance between effector and regulatory cell responses. Here, we have investigated the role of OX40 in influencing the balance between conventional T cells and Foxp3+ regulatory T (T reg) cells. Under steady-state conditions, OX40 was required by T reg cells for their accumulation in the colon, but not peripheral lymphoid organs. Strikingly, under inflammatory conditions OX40 played an essential role in T reg cell-mediated suppression of colitis. OX40(-/-) T reg cells showed reduced accumulation in the colon and peripheral lymphoid organs, resulting in their inability to keep pace with the effector response. In the absence of OX40 signaling, T reg cells underwent enhanced activation-induced cell death, indicating that OX40 delivers an important survival signal to T reg cells after activation. As OX40 also promoted the colitogenic Th1 response, its expression on T reg cells may be required for effective competition with OX40-dependent effector responses. These results newly identify a key role for OX40 in the homeostasis of intestinal Foxp3+ T reg cells and in suppression of colitis. These fi ndings should be taken into account when considering OX40 blockade for treatment of IBD. |
