T cell immunity after a viral infection versus T cell tolerance induced by soluble viral peptides.
The fate of in vivo activated CD8+ cytotoxic T cells was studied in transgenic mice expressing a T cell receptor (TCR) specific for the lymphocytic choriomeningitis virus (LCMV) glycoprotein peptide 33-41 presented by major histocompatibility complex (MHC) class I molecules. LCMV infection of TCR transgenic mice induced LCMV-specific effector and memory T cells whereas injection of soluble LCMV glycoprotein peptide 33-41 resulted in tolerance by peripheral deletion and anergy of LCMV-specific T cells after an initial expansion phase. Similarly, LCMV peptide 33-41-specific tolerance could be achieved in normal C57BL/6 mice and was not abrogated by an LCMV infection. These results obtained with a classically MHC-restricted peptide antigen parallel previous findings with retroviral or bacterial superantigens and indicate a possibility to modulate specifically mature peripheral cytotoxic T lymphocytes in vivo.
Kyburz
D
D
Institute of Experimental Immunology, University of Zürich, Switzerland.
Aichele
P
P
Speiser
D E
DE
Hengartner
H
H
Zinkernagel
R M
RM
Pircher
H
H
D000818:Animals; D016923:Cell Death; D002478:Cells, Cultured; D006801:Humans; D007108:Immune Tolerance; D008212:Lymphocyte Depletion; D008217:Lymphocytic choriomeningitis virus / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D008822:Mice, Transgenic; D010446:Peptide Fragments / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000235:genetics; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology* / Q000502:physiology; D014764:Viral Proteins / Q000276:immunology*
D010446:Peptide Fragments; D011948:Receptors, Antigen, T-Cell; D014764:Viral Proteins