| First Author | Herz U | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 9 | Pages | 3028-34 |
| PubMed ID | 10508277 | Mgi Jnum | J:57692 |
| Mgi Id | MGI:1345552 | Doi | 10.1002/(SICI)1521-4141(199909)29:09<3028::AID-IMMU3028>3.0.CO;2-J |
| Citation | Herz U, et al. (1999) Impact of V beta 8+/+ T cells on the development of increased airway reactivity and IgE production in SJL mice. Eur J Immunol 29(9):3028-34 |
| abstractText | SJL mice have been extensively characterized as low-responder animals in terms of IgE-dependent immediate-type hypersensitivity responses. Since these mice are genetically deficient in certain TCR Vbeta gene segments, we asked whether this might be the reason for the low-responder status. Specifically in H-2d mice the TCR-Vbeta8.2 gene element has been shown to play an important role in Th2 immune responses to ovalbumin (OVA). Utilizing a TCR Vbeta8. 2-transgenic SJL (SJL Vbeta8+/+) mouse, we examined whether the H-2s -bearing low-responder mouse could be converted into a high-responder animal. Remarkably, non-sensitized SJL Vbeta8+/+ mice demonstrated strongly elevated levels of total IgE antibody. Mitogen-stimulated T cells from these mice released high amounts of IL-4 as compared to SJL wild-type (wt) mice. In addition, sensitization to OVA via the airways resulted in the development of increased airway responsiveness in SJL Vbeta8+/+ mice, but not in SJL wt animals. The results indicate that the capacity to produce IgE and IL-4 and to develop increased airway responsiveness can be restored in SJL wt mice by introducing the Vbeta8.2 gene segment into the TCR repertoire. |
