| Autor: |
Gültner, Sandra, Kuhlmann, Tanja, Hesse, Amke, Weber, Jan P., Riemer, Constanze, Baier, Michael, Hutloff, Andreas |
| Zdroj: |
European Journal of Immunology; Dec2010, Vol. 40 Issue 12, p3403-3412, 10p |
| Abstrakt: |
The αLβ2-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-γ 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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