Immune down-regulation and peripheral deletion of CD8 T cells does not require TNF receptor-ligand interactions nor CD95 (Fas, APO-1).

Abstract

TNF receptor-ligand interactions and CD95 (Fas / APO-1) have been demonstrated to be involved in activation-induced death of mature T cells. Here, we examined the role of these molecules in the murine model of lymphocytic choriomeningitis virus (LCMV) infection using LCMV TCR transgenic (tg) mice lacking TNF, TNF receptor I (TNFR1), CD95 or both TNFR1 and CD95. This report demonstrates that neither TNF receptor-ligand interactions nor CD95 was required for down-regulation of LCMV-specific CD8 T cells following acute LCMV infection in vivo. Even LCMV-specific CD8 T cells lacking both TNFR1 and CD95 molecules declined after the acute phase of the infection with normal kinetics. Furthermore, peripheral deletion of LCMV-specific CD8 T cells induced by LCMV peptide injection or by adoptive transfer of tg spleen cells expressing the corresponding LCMV epitope was not impaired in mice lacking TNF, TNFR1 and / or CD95. Our data speak against an indispensable role of these molecules in antigen-induced apoptosis of CD8 T cells in vivo and suggest that T cell homeostasis after antigen challenge is controlled by additional mechanisms.

• Authors: A Reich, H Körner, J D Sedgwick, H Pircher
• Journal: European journal of immunology (Eur J Immunol) Vol. 30 Issue 2 Pg. 678-82 (Feb 2000) ISSN: 0014-2980 [Print] Germany
• PMID: 10671226 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antigens, CD
• Receptors, Antigen, T-Cell
• Receptors, Tumor Necrosis Factor
• Receptors, Tumor Necrosis Factor, Type I
• fas Receptor

Topics

• Animals
• Antigens, CD (immunology)
• Apoptosis (genetics, immunology)
• CD8-Positive T-Lymphocytes (immunology)
• Down-Regulation (immunology)
• Mice
• Mice, Transgenic
• Receptors, Antigen, T-Cell (genetics, immunology)
• Receptors, Tumor Necrosis Factor (immunology)
• Receptors, Tumor Necrosis Factor, Type I
• Signal Transduction (immunology)
• fas Receptor (immunology)