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*
Section of Immunobiology and
Section of Digestive Diseases, Yale University Medical School, New Haven, CT 06520
The lack of CD95 in mice is associated with an accumulation of
TCR
ß+ CD4-CD8-
(double-negative (DN)) cells in the lymph nodes (LNs) and other organs.
To test the hypothesis that these DN cells arise from
TCRß+CD8+ cells after activation via the
TCR, we have crossed an MHC class I-restricted TCR transgene (tg) onto
the lpr genotype to generate two TCR-transgenic
experimental groups, TCRtg+ lpr/+
(CD95-intact) and TCRtg+ lpr/lpr
(CD95-deficient). Specific peptide administration resulted in
peripheral deletion of TCRß cells from the LNs of CD95-intact and
CD95-deficient mice. On day 3 after peptide administration in the
CD95-deficient but not the CD95-intact mice, there was a ninefold
increase in the percentage of DN cells in the LN; this increase
returned to control levels by day 10. Peripheral deletion was
associated with an accumulation of
TCRß+CD8high cells in the livers of
mice of both genotypes by day 3, which returned to control levels by
day 10 without an increase in the percentage or total number of DN
cells. Our data show that the in vivo stimulation of
TCRß+CD8+ cells in the absence of CD95
results in an initial accumulation and an eventual loss of DN cells.
This identifies a role for CD95 after TCRß stimulation in the
efficient removal of TCRß+CD8+ cells after
the down-regulation of CD8. CD95 is not essential for this process,
because other mechanisms can compensate, but such mechanisms are less
efficient in the LN.
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