The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20510iti2
The Journal of Experimental Medicine, Vol. 205, No. 10, 2182-
The Rockefeller University Press, 0022-1007 $30.00
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IN THIS ISSUE

 Tardy DCs to the (Th1) rescue
Figure 1
Delayed development of interferon-{gamma}–producing Th1 cells in newborns.

In newborns, the sluggish appearance of one cell population means death to another, according to Lee et al. on page 2269. These results may help explain why newborns are highly susceptible to certain infections.

Newborn mice exposed to antigen respond by activating both T helper (Th)-1 and Th2 cells. Yet a second exposure causes allergy-promoting Th2 cells to thrive but microbe-fighting Th1 cells to die. Previous work by this group showed that antigen exposure during the first few days of life caused Th1 cells to express the cytokine receptor chain IL-13R{alpha}1, a receptor not commonly found on these cells, which then teamed up with the IL-4R{alpha} chain. The resulting heteroreceptor induced Th1 cell death when triggered by Th2-promoting IL-4 during secondary antigen exposure.

At six days of age, the authors now show, Th1 cells had a reversal of fortune. The turning point was marked by the appearance of a subset of antigen-presenting CD8{alpha}+ dendritic cells (DCs) that churned out life-saving IL-12. Giving newborns extra IL-12, which is feebly produced before day 6, or providing them with IL-12–producing DCs blunted the expression of IL-13R{alpha}1 and rescued the Th1 cells. What delays the development of this DC population relative to other subsets remains unknown. RB



Rebecca Blank

rebecca.blank{at}gmail.com


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This Article
Right arrow Full Text (PDF, 1094K)
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Right arrow Alert me when this article is cited
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Right arrow Email this article
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Right arrow Download to citation manager
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Google Scholar
Right arrow Articles by Blank, R.
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Right arrow Articles by Blank, R.
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