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

. 2012 Apr 9;209(4):761–774. doi: 10.1084/jem.20112095

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

© 2012 Reantragoon et al.

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 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

PMC Copyright notice

Figure 7. — The effect of mutation of MR1 residues on MAIT TCR activation. (A) 13 mutant MR1, as well as wild-type MR1 (C1R.WT) and parental C1R, cell lines were either not infected (open bars) or infected (shaded bars) with S. typhimurium at a multiplicity of infection (MOI) of 1. After infection, Jurkat.TRBV 20, Jurkat.TRBV 6–1, or Jurkat.TRBV 6–4 cell lines were then added for 16 h before measurement of increase in CD69 surface expression (MFI) by staining and flow cytometric analysis. This experiment was performed twice with similar results. Mutant Arg167Ala MR1 C1R cells activated Jurkat.MAIT cells similarly to wild-type MR1 C1R cells (not depicted). The experiment was also performed at an MOI of 10 with similar results (not depicted). (B) The effects of the MR1 mutants were mapped onto the human MR1 homology model. Mutations that had no impact on MAIT TCR activation is shown in gray; impact on autoreactivity is shown in orange; mutants that markedly reduced MAIT TCR activation are shown in red.