| First Author | Lee SJ | Year | 2013 |
| Journal | Eur J Immunol | Volume | 43 |
| Issue | 7 | Pages | 1839-48 |
| PubMed ID | 23640752 | Mgi Jnum | J:201017 |
| Mgi Id | MGI:5510642 | Doi | 10.1002/eji.201242842 |
| Citation | Lee SJ, et al. (2013) 4-1BB signal stimulates the activation, expansion, and effector functions of gammadelta T cells in mice and humans. Eur J Immunol 43(7):1839-48 |
| abstractText | We show here that the expression of 4-1BB is rapidly induced in gammadelta T cells following antigenic stimulation in both mice and humans, and ligation of the newly acquired 4-1BB with an agonistic anti-4-1BB augments cell division and cytokine production. We further demonstrate that gammadelta rather than alphabeta T cells protect mice from Listeria monocytogenes (LM) infection and 4-1BB stimulation enhances the gammadelta T-cell activities in the acute phase of LM infection. IFN-gamma produced from gammadelta T cells was the major soluble factor regulating LM infection. Vgamma1(+) T cells were expanded in LM-infected mice and 4-1BB signal triggered an exclusive expansion of Vgamma1(+) T cells and induced IFN-gamma in these Vgamma1(+) T cells. Similarly, 4-1BB was induced on human gammadelta T cells and shown to be fully functional. Combination treatment with human gammadelta T cells and anti-hu4-1BB effectively protected against LM infection in human gammadelta T cell-transferred NOD-SCID mice. Taken together, these data provide evidence that the 4-1BB signal is an important regulator of gammadelta T cells and induces robust host defense against LM infection. |
