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Correction for Traidl-Hoffmann et al., J. Exp. Med. 201 (4) 627-636.
Published 18 April 2005. doi:10.1084/jem.20041065040105c
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 8, 1347-1347
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CORRECTION



Claudia Traidl-Hoffmann, Valentina Mariani, Hubertus Hochrein, Kathrin Karg, Hermann Wagner, Johannes Ring, Martin J. Mueller, Thilo Jakob, and Heidrun Behrendt


Vol. 201, No. 4, February 21, 2005. Pages 627–636.

The authors regret that an inaccurate version of Fig. 4 appears in the original article. The correct version of Fig. 4 and its legend appear below.



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Figure 4. DCs matured in the presence of Bet.-APE display reduced Th1- and increased Th2-polarizing capacity. DCs were left untreated or stimulated with Bet.-APE (3 mg/ml) in the presence or absence of LPS (100 ng/ml). After 24 h DCs were washed and cocultured with CD4+CD45RA+ allogenic T cells (DC/T cell ratio 1:4) that were expanded for 12 d in the presence of IL-2. T cell polarization was determined by analyzing intracellular IFN-{gamma} and IL-4 accumulation via flow cytometry after restimulation with PMA and ionomycin in the presence of brefeldin A during the last 2 h of stimulation. To address, if the Bet.-APE–dependent Th2 polarization could be reverted by exogenous IL-12, hrIL-12 (10 ng/ml) was added at the beginning of the coculture of Bet.-APE/LPS-treated DCs and T cells. Representative experiment of n = 3–6 (compare Table I). To explore the role of IL-4 in the Th2 polarization induced by Bet.-APE–treated DCs, IL-4–neutralizing antibodies (10 µg/ml) were added at the beginning of the DC/T cell coculture. Representative experiment of n = 3.

 


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This Article
Right arrow Full Text (PDF, 64K)
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