| First Author | Gültner S | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 12 | Pages | 3403-12 |
| PubMed ID | 21108463 | Mgi Jnum | J:174580 |
| Mgi Id | MGI:5139988 | Doi | 10.1002/eji.201040576 |
| Citation | Gultner S, et al. (2010) Reduced Treg frequency in LFA-1-deficient mice allows enhanced T effector differentiation and pathology in EAE. Eur J Immunol 40(12):3403-12 |
| abstractText | The alphaLbeta2-integrin LFA-1 (CD11a/CD18) is known as an important molecule for leukocyte migration. However, the precise role of LFA-1 in the pathogenesis of EAE has so far remained unclear. We describe here the disease development in LFA-1(-/-) mice compared with WT controls. Ablation of LFA-1 resulted in more severe EAE with increased demyelination and increased numbers of myelin oligodendrocyte glycoprotein-reactive CD4(+) T cells in the CNS. However, the production of the pro-inflammatory cytokines IL-17 and IFN-gamma was unchanged on the level of antigen-specific T cells. Interestingly, LFA-1-deficient mice showed a clearly reduced frequency of Treg in the inflamed CNS. Moreover, Treg counts in spleens and thymi of unimmunized LFA-1(-/-) mice were lower in comparison to the WT controls, indicating an impairment of Treg generation. In combination, these results suggest a substantial role of LFA-1 in Treg generation and subsequent expansion of effector T cells and highlight the importance of Treg in limiting EAE. |
