These authors contributed equally to this work.
Salmonella polarises peptide-MHC-II presentation towards an unconventional Type B CD4+ T-cell response
Article first published online: 18 FEB 2013
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
European Journal of Immunology
Volume 43, Issue 4, pages 897–906, April 2013
How to Cite
Jackson, N. P., Kang, Y. H., Lapaque, N., Janssen, H., Trowsdale, J. and Kelly, A. P. (2013), Salmonella polarises peptide-MHC-II presentation towards an unconventional Type B CD4+ T-cell response. Eur. J. Immunol., 43: 897–906. doi: 10.1002/eji.201242983
- Issue published online: 16 APR 2013
- Article first published online: 18 FEB 2013
- Accepted manuscript online: 14 JAN 2013 09:03AM EST
- Manuscript Accepted: 8 JAN 2013
- Manuscript Revised: 3 DEC 2012
- Manuscript Received: 13 SEP 2012
- Royal Society of New Zealand Rutherford Foundation
- Wellcome Trust
- National Institute for Health Research (NIHR)
- Cambridge Biomedical Research Centre
As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors.
Figure 1: Representative gating strategies for MelJuSo, HeLa-CIITA and BMDCs (A) and flow cytometry plots showing representative MHC-II down-regulation by Salmonella for each HeLa-HLA-DR3 transfectant used in Figure 2 (B)
Figure 2: Salmonella does not down-regulate MHC-II in human monocyte-derived macrophage or a murine macrophage cell line (RAW264.7-CIITA)
Figure 3: Relationship between BMDC: T hybridoma cell ratio and IL-2 response
Figure 4: Transwell experiment showing exposure to Salmonella is sufficient to enhance presentation of exogenous peptide to Type B T cells
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.