A r t i c l e A m e n d m e n t s2At the request of the corresponding author, John W. Hollingsworth, and the last author, David A. Schwartz, the JCI is retracting this paper.Following an inquiry at Duke University, Drs. Hollingsworth and Schwartz were informed that the flexiVent data depicted in Figure 1A and Supplemental Figure 1A provided by the animal pulmonary physiology laboratory at Duke University may have been unreliable. Dr. Schwartz therefore repeated the experiments shown in Figure 1A using different flexiVent equipment with a limited number of experimental animals and was unable to replicate the airway hyperresponsiveness findings. The authors have stated that the other findings presented in the article were generated and analyzed in Dr. Schwartz's laboratory and are not affected by the unreliable flexiVent data produced by the animal pulmonary physiology laboratory at Duke University. In the left panel of Figure 8A, the P value for comparing KO Ang II with KO Ang II-Cl10400 was incorrect in the print version and the original online version of this article; a correct version of the latter has since been published. The correct figure panel is below. ErratumThe JCI regrets the error.

A r t i c l e A m e n d m e n t s2At the request of the corresponding author, John W. Hollingsworth, and the last author, David A. Schwartz, the JCI is retracting this paper.Following an inquiry at Duke University, Drs. Hollingsworth and Schwartz were informed that the flexiVent data depicted in Figure 1A and Supplemental Figure 1A provided by the animal pulmonary physiology laboratory at Duke University may have been unreliable. Dr. Schwartz therefore repeated the experiments shown in Figure 1A using different flexiVent equipment with a limited number of experimental animals and was unable to replicate the airway hyperresponsiveness findings. The authors have stated that the other findings presented in the article were generated and analyzed in Dr. Schwartz's laboratory and are not affected by the unreliable flexiVent data produced by the animal pulmonary physiology laboratory at Duke University. In the left panel of Figure 8A, the P value for comparing KO Ang II with KO Ang II-Cl10400 was incorrect in the print version and the original online version of this article; a correct version of the latter has since been published. The correct figure panel is below. ErratumThe JCI regrets the error.

Ligand-induced BCR association with detergent-resistant plasma membrane compartments (lipid rafts) has been argued to be essential for initiating and/or sustaining Igα/Igβ-dependent BCR signaling. Because a fraction of the BCR and an even larger fraction of the preBCR associates with lipid rafts in the apparent absence of ligand stimulation, it has been proposed that raft-associated receptor complexes mediate the ligand-independent basal signaling events observed in resting B lineage cells. However, there is no direct evidence that localization of Igα/Igβ-containing complexes to detergent-resistant membrane compartments is absolutely required for the signaling events that drive B cell development. To address these issues we have designed surrogate preBCR/Igα/Igβ complexes that are incapable of ligand-induced aggregation and that are preferentially targeted to either raft or nonraft compartments. An analysis of their ability to promote the preBCR-dependent proB→preB cell transition of murine B cell progenitors revealed that expression of these surrogate receptor complexes at levels that approximate that of the conventional preBCR can drive B cell development in a manner independent of both aggregation and lipid raft localization.

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