Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2006 Mar 20;203(3):553–561. doi: 10.1084/jem.20052438

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2006, The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Figure 6. — Loss of IgG2a and 2b autoantibodies in TLR9-deficient mice was B cell autonomous. (A) Naive splenic B cells from the indicated genotypes were stimulated with 15 μg/ml CpG1826, 10 μg/ml anti-CD40, and 10 ng/ml rmIL-4 in vitro for 5 d and total Ig subclass concentrations in the supernatants were determined. Class switching to IgM was unchanged and to IgG1 increased in TLR9-deficient backgrounds. In contrast, switching to IgG2a, 2b, and 3 was significantly impaired. (B) T-bet mRNA is not induced by CpG stimulation of B cells in the TLR9-deficient background. A portion of the cells in (A) were collected after 12 h of the indicated stimulation. mRNA and cDNA were prepared and used for real-time PCR with specific primers for T-bet and β-actin as an internal control. The ratio between TLR9-sufficient and -deficient B cells for T-bet mRNA was calculated after normalizing for β-actin. nd, not detected. Results from three independent experiments are shown as mean ± SD.