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Open Access

Correction

Correction: Innate Immune Signaling Induces Interleukin-7 Production from Salivary Gland Cells and Accelerates the Development of Primary Sjögren’s Syndrome in a Mouse Model

  • The PLOS ONE Staff

Figure 1 is a duplicate of Figure 2. The authors have provided a corrected Figure 1 here.

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Figure 1. Poly I:C induces IL-7 expression in the submandibular glands.

(A) Real-time PCR analysis of gene expression in submandibular glands from C57BL/6 mice 6 hours post poly I:C injection, presented relative to that of β-actin. Data are the average of analyses of 6 individual mice (3 mice per experiment, total 2 independent experiments). (B) Immunofluorescence staining of IL-7 in submandibular gland sections from C57BL/6 mice 24 hourse post poly I:C injection. Differential interference contrast (DIC) image of the same sample is also shown. Data are representative of analyses of 6 individual mice (3 mice per experiment, total 2 independent experiments). (C) C57BL/6 mice were pretreated with anti-IFNAR1 or anti-IFN-γ 2 hours prior to poly I:C injection. After 6 hours, relative IL-7 mRNA levels in lung tissue were measured by real-time RT-PCR. Data are from analyses of 6 individual mice (2 mice per experiment, total 3 independent experiments).

https://doi.org/10.1371/journal.pone.0077605.g001

Reference

  1. 1. Jin J-O, Shinohara Y, Yu Q (2013) Innate Immune Signaling Induces Interleukin-7 Production from Salivary Gland Cells and Accelerates the Development of Primary Sjögren’s Syndrome in a Mouse Model. PLoS ONE 8(10): e77605

Citation: The PLOS ONE Staff (2014) Correction: Innate Immune Signaling Induces Interleukin-7 Production from Salivary Gland Cells and Accelerates the Development of Primary Sjögren’s Syndrome in a Mouse Model. PLoS ONE 9(9): e108573. https://doi.org/10.1371/journal.pone.0108573

Published: September 16, 2014

Copyright: © 2014 The PLOS ONE Staff. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.