| First Author | Albrecht I | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 11 | Pages | 2993-3006 |
| PubMed ID | 21061432 | Mgi Jnum | J:167626 |
| Mgi Id | MGI:4868654 | Doi | 10.1002/eji.201040936 |
| Citation | Albrecht I, et al. (2010) Persistence of effector memory Th1 cells is regulated by Hopx. Eur J Immunol 40(11):2993-3006 |
| abstractText | Th1 cells are prominent in inflamed tissue, survive conventional immunosuppression, and are believed to play a pivotal role in driving chronic inflammation. Here, we identify homeobox only protein (Hopx) as a critical and selective regulator of the survival of Th1 effector/memory cells, both in vitro and in vivo. Expression of Hopx is induced by T-bet and increases upon repeated antigenic restimulation of Th1 cells. Accordingly, the expression of Hopx is low in peripheral, naive Th cells, but highly up-regulated in terminally differentiated effector/memory Th1 cells of healthy human donors. In murine Th1 cells, Hopx regulates the expression of genes involved in regulation of apoptosis and survival and makes them refractory to Fas-induced apoptosis. In vivo, adoptively transferred Hopx-deficient murine Th1 cells do not persist. Consequently, they cannot induce chronic inflammation in murine models of transfer-induced colitis and arthritis, demonstrating a key role of Hopx for Th1-mediated immunopathology. |
