Evidence for Fas-dependent and Fas-independent mechanisms in the pathogenesis of experimental autoimmune encephalomyelitis
| Autor: | B N, Dittel, R M, Merchant, C A, Janeway |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Mice
Inbred MRL lpr Encephalomyelitis Autoimmune Experimental Fas Ligand Protein Membrane Glycoproteins Receptors Antigen T-Cell alpha-beta T-Lymphocytes Mice Transgenic Myelin Basic Protein Th1 Cells Ligands Adoptive Transfer Peptide Fragments Cell Line Mice Inbred C57BL Mice Antigens Surface Animals Cytokines Female Genetic Predisposition to Disease fas Receptor Crosses Genetic |
| Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 162(11) |
| ISSN: | 0022-1767 |
| Popis: | To determine whether Fas or Fas ligand (FasL) plays a role in susceptibility to experimental autoimmune encephalomyelitis (EAE), we bred a TCR transgenic mouse specific for the Ac1-11 peptide of myelin basic protein to mice with inactivating mutations in Fas (lpr) or FasL (gld). Disease induction by peptide immunization in such mice produced similar disease scores, demonstrating that Fas/FasL interactions were not necessary to generate EAE. However, adoptive transfer experiments showed evidence that these interactions can play a role in the pathogenesis of EAE, shown most dramatically by the absence of disease following transfer of cells from a normal myelin basic protein TCR transgenic mouse into a Fas-deficient lpr recipient. Furthermore, transfer of cells lacking FasL (gld) into normal or gld recipients gave a diminished disease score. Thus, Fas/FasL interactions can play a role in the pathogenesis of EAE, but they are not required for disease to occur. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|