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Department of Microbiology, University of Tennessee, Knoxville, TN 37996
In recent years, it has become clear that neonatal exposure to Ag
induces rather than ablates T cell immunity. Moreover, rechallenge with
the Ag at adult age can trigger secondary responses that are distinct
in the lymph node vs the spleen. The question addressed in this report
is whether organ-specific secondary responses occur as a result of the
diversity of the T cell repertoire or could they arise with homogeneous
TCR-transgenic T cells. To test this premise, we used the OVA-specific
DO11.10 TCR-transgenic T cells and established a neonatal T cell
transfer system suitable for these investigations. In this system,
neonatal T cells transferred from 1-day-old DO11.10/SCID mice into
newborn (1-day-old) BALB/c mice migrate to the host’s spleen and
maintain stable frequency. The newborn BALB/c hosts were then given
Ig-OVA, an Ig molecule carrying the OVA peptide, and challenged with
the OVA peptide in CFA at the age of 7 wk; then their secondary
responses were analyzed. The findings show that the lymph node T cells
were deviated and produced IL-4 instead of IFN-
and the splenic T
cells, although unable to proliferate or produce IFN-, secreted a
significant level of IL-2. Supply of exogenous IL-12 during Ag
stimulation restores both proliferation and IFN- production by the
splenic T cells. This restorable form of splenic unresponsiveness
referred to as IFN--dependent anergy required a transfer of a high
number of neonatal DO11.10/SCID T cells to develop. Thus, the frequency
of neonatal T cell precursors rather than repertoire diversity exerts
control on the development of organ-specific neonatal
immunity.
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