Regulation of Fas and FasL expression on rat Schwann cells

Gisela Wohlleben, Saleh M. Ibrahim, Jens Schmidt, Klaus V. Toyka, Hans Peter Hartung, Ralf Gold*

*Corresponding author for this work
37 Citations (Scopus)


Although the PNS belongs to the immune privileged sites, it can become a target of immune attacks by invading T cells, causing inflammation and destruction. Yet the PNS also has a protective potential by eliminating the inflammatory cells via apoptosis. In analogy with other immune-protected sites, participation of the apoptosis-inducing Fas/FasL molecules could play an important role. To assess the possible involvement of the Fas/FasL system in T-cell apoptosis in the PNS of the rat, we characterized Fas and FasL expression on neonatal rat Schwann cells (SC) in vitro. Cells were stimulated in vitro with interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), or a combination of both. We observed upregulation of FasL expression under the influence of IFN-γ, while adding TNF-α alone to the culture medium had no effect. IFN-γ and TNF-α acted synergistically, leading to an increased FasL expression that reached its maximum 70 h after cytokine exposure, as shown by FACS analysis, SDS-PAGE, and Western blot. Fas expression on untreated SC showed fluctuating levels, while addition of IFN-γ and TNF-α suppressed Fas expression completely. These findings are in accord with recently published results showing Fas and FasL expression on malignant human cells, derived from brain tumors and upregulation of FasL on astrocytes after exposure to IFN-γ and TNF-α. Furthermore, FasL-expressing SC could be revealed by immunostaining of sciatic nerve from Lewis rats suffering from experimental autoimmune neuritis (EAN). We suggest that Fas/FasL expression on SC may contribute to the elimination of invading autoreactive T cells in the PNS in concert with other immune defense mechanisms. (C) 2000 Wiley-Liss, Inc.

Original languageEnglish
Issue number4
Pages (from-to)373-381
Number of pages9
Publication statusPublished - 2000

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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