| First Author | Galicia G | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 12 | Pages | 3404-12 |
| PubMed ID | 19795414 | Mgi Jnum | J:155484 |
| Mgi Id | MGI:4414601 | Doi | 10.1002/eji.200939291 |
| Citation | Galicia G, et al. (2009) Haptoglobin deficiency facilitates the development of autoimmune inflammation. Eur J Immunol 39(12):3404-12 |
| abstractText | Haptoglobin (HP) is an acute phase protein synthesized by liver cells in response to IL-6. HP has been demonstrated to modulate the immune response and to have anti-inflammatory activities. To analyze HP's effect on autoimmune inflammation, we here studied the course of EAE induced by immunization of Hp knockout (Hp(-/-)) and syngeneic WT mice with myelin oligodendrocyte glycoprotein peptide (MOG(35-55)). Hp(-/-)mice suffered from a more severe disease that was associated with increased expression of IL-17A, IL-6, and IFN-gamma mRNA in the CNS and with a denser cellular infiltrate in the spinal cord. During the recovery phase, a significantly higher number of myeloid DC, CD8+ cells, IL-17+ CD4+ and IFN-gamma+ CD4+ cells persisted in the CNS of Hp(-/-) mice. Absence of HP affected the priming and differentiation of T cells after MOG(35-55) immunization, as levels of Th2 cytokines produced in response to MOG stimulation by Hp(-/-) T cells were reduced. These results suggest that HP plays a modulatory and protective role on autoimmune inflammation of the CNS. |
