| First Author | Alimi E | Year | 1998 |
| Journal | Eur J Immunol | Volume | 28 |
| Issue | 1 | Pages | 201-8 |
| PubMed ID | 9485200 | Mgi Jnum | J:45901 |
| Mgi Id | MGI:1196682 | Doi | 10.1002/(SICI)1521-4141(199801)28:01<201::AID-IMMU201>3.0.CO;2-N |
| Citation | Alimi E, et al. (1998) Experimental autoimmune thyroiditis (EAT) in mice lacking the IFN-gamma receptor gene. Eur J Immunol 28(1):201-8 |
| abstractText | To investigate the role of interferon-gamma (IFN-gamma) in experimental autoimmune thyroidits (EAT), H-2k mice with a disrupted IFN-gamma receptor (IFN-gamma R) gene were immunized with porcine thyroglobulin (pTg). We observed that EAT occurred on day 19 and remitted on day 35 in IFN-gamma R-deficient (IFN-gamma R(0/0)) mice, whereas in wild-type mice, EAT occurred on day 21 and remitted on day 42-49. Moreover, EAT in the mutant mice was attenuated and accompanied by diminished Tg-specific cytotoxic and proliferative responses and decreased titers of anti-Tg antibodies, notably of the IgG2a and IgG2b isotypes. In contrast, Tg-specific IgG1 was increased in the IFN-gamma R(0/0) mice. In supernatants from T cells further stimulated in vitro by Tg, IFN-gamma levels were higher in IFN-gamma R(0/0) than in wild-type mice throughout the course of the disease, whereas interleukin-10 was transiently increased prior to EAT onset in both groups of mice. Finally, using IFN-gamma R(0/0) mice, we demonstrate that induction of EAT does not require an intact IFN-gamma system, while progression to full-blown disease depends on the action of IFN-gamma. |
