International Immunology Advance Access published online on November 15, 2005
International Immunology, doi:10.1093/intimm/dxh350
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Ashworth Laboratories, West Mains Road, Edinburgh EH9 3JT, UK
* To whom correspondence should be addressed. B cells act as efficient antigen-presenting cells if they acquire antigen via membrane-bound Ig [termed the B cell receptor (BCR)]. Ligation of the BCR leads to antigen internalization, processing and presentation to CD4+ T cells in association with MHC class II molecules. Ligation of the BCR also leads to the generation of activation signals. One short-term consequence of this is the up-regulation of co-stimulatory molecule expression by the B cell, allowing full T cell activation. Other antigen receptors expressed by B cells can also mediate efficient antigen presentation to CD4+ T cells. Ligating one such receptor, complement receptor 2 (CR2), has also been described to induce co-stimulatory molecule expression. If correct, this may have serious consequences for ensuring the specificity of the resultant B cell response. We have therefore investigated the effects of ligating both the BCR and CR2 independently of each other, as well as with reagents to cross-link the two receptors, in order to clarify these findings. In contrast to the effects seen upon BCR ligation, we find no evidence for co-stimulatory molecule up-regulation following CR2 ligation. As antigen presentation in the absence of co-stimulation may lead to the induction of tolerogenic or regulatory signals being delivered to T cell populations, these findings imply that the role of CR2 in B cell-mediated antigen presentation is different from that of the BCR.
Received March 17, 2005
Accepted October 6, 2005
Article
Lack of induced co-stimulation as a result of complement receptor 2 (CR2) ligation on mouse splenic B cells
Sheila L. Brown 1,
Denise V. Barrault 2,
Alex Phythian-Adams 1,
and
Andrew M. Knight 3 *
2 Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Ashworth Laboratories, West Mains Road, Edinburgh EH9 3JT, UK; Present address: Lab901 Ltd, Unit 53, IMEX Business Centre, Bilston Glen Industrial Estate, Loanhead, Midlothian EH20 9LZ, UK
3 Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Ashworth Laboratories, West Mains Road, Edinburgh EH9 3JT, UK; Present address: School of Surgical and Reproductive Sciences, Faculty of Medical Sciences, University of Newcastle upon Tyne, 3rd Floor, William Leech Building, Framlington Place, Newcastle upon Tyne NE2 4HH, UK
Andrew M. Knight, E-mail: andrew.knight{at}ncl.ac.uk
![]()
Abstract ![]()
CiteULike
Connotea
Del.icio.us What's this?