| First Author | Savinov AY | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 11 | Pages | 6637-43 |
| PubMed ID | 11714835 | Mgi Jnum | J:72818 |
| Mgi Id | MGI:2153642 | Doi | 10.4049/jimmunol.167.11.6637 |
| Citation | Savinov AY, et al. (2001) IFN-gamma Affects Homing of Diabetogenic T Cells. J Immunol 167(11):6637-43 |
| abstractText | IFN-gamma is a cytokine with pleiotropic functions that participates in immune and autoimmune responses. The lack of IFN-gamma is known to delay the development of autoimmune diabetes in nonobese diabetic (NOD) mice. Splenocytes from diabetic NOD and IFN-gamma knockout (KO) NOD mice transfer diabetes into NOD recipients equally well. However, adoptive transfer of diabetogenic T cells from NOD mice into NOD.IFN-gamma-KO or NOD mice lacking beta-chain of IFN-gamma receptor (NOD.IFN-gammaRbeta-KO) appeared to be much less efficient. We found that IFN-gamma influences the ability of diabetogenic cells to penetrate pancreatic islets. Tracing in vivo of insulin-specific CD8(+) T cells has shown that homing of these cells to the islets of Langerhans was affected by the lack of IFN-gamma. While adhesion of insulin-specific CD8(+) cells to microvasculature was normal, the diapedesis was significantly impaired. This effect was reversible by treatment of the animals with rIFN-gamma. Thus, IFN-gamma may, among other effects, influence immune and autoimmune responses by supporting the homing of activated T cells. |
