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Department of Microbiology and Immunology, University of Miami Medical School, Miami, FL 33136
It is well established that murine neonates are biased toward Th2
responses. Th2-dominant responses are observed following immunization
with a variety of Ags, using different carrier/adjuvant systems, and
are seen in both BALB/c and C57BL/6 mice. Therefore, Th2 skewing
appears to be a universal phenomenon unique to the neonatal period. One
important question about this phenomenon is whether these responses are
due to T cell intrinsic properties or are regulated by the neonatal
environment. Here we have addressed this issue by transferring neonatal
or adult CD4+ lymph node cells to adoptive adult
recombinase-activating gene 2-/- hosts and studied the
development of Th responses. Neonatal CD4+ cells were
highly deficient in the development of both primary and secondary
Ag-specific Th1 responses. This did not appear to be due to anergy of a
developed population, since exogenous IL-2 only marginally increased
production of the Th1 cytokine IFN-
. This profound Th1 deficiency
was observed despite similar proliferation by neonatal and adult cells
within the recombinase-activating gene 2-/- hosts.
Moreover, neonatal CD4+ cells up-regulated activation
markers in a manner similar to adult CD4+ cells. Therefore,
although their proliferation and phenotypic maturation proceeded
normally, neonatal CD4+ cells appeared to be intrinsically
deficient in the functional maturation of Th1 lineage cells. These
results offer a candidate explanation for the reduced graft-vs-host
responses observed following transplantation of cord blood cells or
murine neonatal lymphoid cells to allogeneic adult
hosts.
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