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CORRESPONDENCE Habib Zaghouani: zaghouanih{at}health.missouri.edu
Primary neonatal T cell responses comprise both T helper (Th) cell subsets, but Th1 cells express high levels of interleukin 13 receptor
1 (IL-13R1), which heterodimerizes with IL-4R. During secondary antigen challenge, Th2-produced IL-4 triggers the apoptosis of Th1 cells via IL-4R/IL-13R1, thus explaining the Th2 bias in neonates. We show that neonates acquire the ability to overcome the Th2 bias and generate Th1 responses starting 6 d after birth. This transition was caused by the developmental maturation of CD8+CD4– dendritic cells (DCs), which were minimal in number during the first few days of birth and produced low levels of IL-12. This lack of IL-12 sustained the expression of IL-13R1 on Th1 cells. By day 6 after birth, however, a significant number of CD8+CD4– DCs accumulated in the spleen and produced IL-12, which triggered the down-regulation of IL-13R1 expression on Th1 cells, thus protecting them against IL-4–driven apoptosis.
R, Fc receptor; Tg, transgenic. H.-H. Lee and C.M. Hoeman contributed equally to this paper.
H.-H. Lee's present address is Division of Immunology, Karp Laboratories, Children's Hospital, Harvard Medical School, Boston, MA 02115.
© 2008 Lee et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
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