This information is current as of October 24, 2017. Correction: IL-33 Signaling Regulates Innate IL-17A and IL-22 Production via Suppression of Prostaglandin E2 during Lung Fungal Infection Jaleesa M. Garth, Kristen M. Reeder, Matthew S. Godwin, Joseph J. Mackel, Chad W. Dunaway, Jonathan P. Blackburn and Chad Steele Why The JI? • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Speedy Publication! 4 weeks from acceptance to publication *average Subscription Permissions Email Alerts Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2017 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Downloaded from http://www.jimmunol.org/ by guest on October 24, 2017 J Immunol 2017; 199:3381; ; doi: 10.4049/jimmunol.1701301 http://www.jimmunol.org/content/199/9/3381 The Journal of Immunology 3381 Corrections Garth, J. M., K. M. Reeder, M. S. Godwin, J. J. Mackel, C. W. Dunaway, J. P. Blackburn, and C. Steele. 2017. IL-33 signaling regulates innate IL-17A and IL-22 production via suppression of prostaglandin E2 during lung fungal infection. J. Immunol. 199: 2140–2148. The authors discovered mislabeled axes in Fig. 6C. Specifically, the y-axis should read “pg/ml (lung digest cells - 48 h)” instead of “IL-22 pg/ml (lung digest cells - 48 h).” In addition, “IL-1a” and “IL-1b” should be included on the x-axis. The corrected version of Fig. 6 is shown below. The figure legend was correct as published and is shown below for reference. The online version of this article has been corrected and now differs from the print version as originally published. We apologize for this oversight. www.jimmunol.org/cgi/doi/10.4049/jimmunol.1701301 Copyright Ó 2017 by The American Association of Immunologists, Inc. 0022-1767/17/$35.00 Downloaded from http://www.jimmunol.org/ by guest on October 24, 2017 FIGURE 6. Increased IL-1R signaling is not the mechanism associated with enhanced PGE2 and IL-22 in Il1rl12/2 mice after A. fumigatus exposure. BL/6 WT and Il1rl12/2 (IL-1R1–deficient) mice were challenged intratracheally with A. fumigatus conidia, and 48 h after exposure, the right lungs were collected and enzymatically digested, and unfractionated lung cells were cultured in triplicate for 24 h. PGE2 levels were quantified in clarified coculture supernatants by enzyme immunoassay (A), and IL-22 levels were quantified in clarified coculture supernatants by ELISA (B). The figures illustrate cumulative data from four independent studies (n 5 1 or 2 mice per group, per study). (C) BL/6 WT mice were challenged with A. fumigatus and administered IL-33 (1 mg in 50 ml) or PBS intratracheally 6 and 24 h later. Forty-eight hours after exposure, the right lungs were collected and enzymatically digested, and unfractionated lung cells were cultured in triplicate for 24 h. IL-1a and IL-1b levels were quantified in clarified coculture supernatants by Bio-Plex. The figure illustrates cumulative data from two independent studies (n 5 1 or 2 mice per group, per study). ***p , 0.001, unpaired two-tailed Student t test.