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J. Exp. Med.,
Volume 188, Number 1, July 1, 1998 71-82
By
§
From the * Emory Vaccine Center, Rollins Research Center, and the Viral infections often induce potent CD8 T cell responses that play a key role in antiviral immunity. After viral clearance, the vast majority of the expanded CD8 T cells undergo apoptosis, leaving behind a stable number of memory cells. The relationship between the CD8 T cells
that clear the acute viral infection and the long-lived CD8 memory pool remaining in the individual is not fully understood. To address this issue, we examined the T cell receptor (TCR)
repertoire of virus-specific CD8 T cells in the mouse model of infection with lymphocytic
choriomeningitis virus (LCMV) using three approaches: (a) in vivo quantitative TCR Department of Microbiology and
Immunology, Emory University, Atlanta, Georgia 30322; the § Centre d'Etudes du Bouchet, 91710 Vert-le-Petit, France; the Unité de Biologie Moléculaire du Gène, Institut Pasteur, 75724 Paris cedex
15, France; and ¶ Epimmune, San Diego, California 92121
chain
V segment and complementarity determining region 3 (CDR3) length repertoire analysis by
spectratyping (immunoscope); (b) identification of LCMV-specific CD8 T cells with MHC
class I tetramers containing viral peptide and costaining with TCR V-specific antibodies; and
(c) functional TCR fingerprinting based on recognition of variant peptides. We compared the
repertoire of CD8 T cells responding to acute primary and secondary LCMV infections, together with that of virus-specific memory T cells in immune mice. Our analysis showed that
CD8 T cells from several V families participated in the anti-LCMV response directed to the
dominant cytotoxic T lymphocyte (CTL) epitope (NP118-126). However, the bulk (~70%) of
this CTL response was due to three privileged T cell populations systematically expanding during
LCMV infection. Approximately 30% of the response consisted of V10+ CD8 T cells with a
chain CDR3 length of nine amino acids, and 40% consisted of V8.1+ ( CDR3 = eight amino
acids) and V8.2+ cells ( CDR3 = six amino acids). Finally, we showed that the TCR repertoire of the primary antiviral CD8 T cell response was similar both structurally and functionally
to that of the memory pool and the secondary CD8 T cell effectors. These results suggest a stochastic selection of memory cells from the pool of CD8 T cells activated during primary infection.
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