Abstract
AimT cells have been attributed an important role in modulating repair responses following vascular injury. The aim of this study was to investigate the role of different T cell subsets in this context.Methods and ResultsA non-obstructive collar was introduced to inflict carotid artery injury in mice and subsequent activation of immune cells in draining lymph nodes and spleen were studied by flow cytometry. Carotid artery injury of wild type mice was associated with mobilization of both Th1 type CD4+IFNγ+ and regulatory CD4+CD25+FoxP3+ T cells in draining lymph nodes. Studies using FoxP3-green fluorescent protein (GFP) transgenic C57/Bl6 mice demonstrated scattered presence of regulatory T cells in the adventitial tissue of injured arteries as well as a massive emigration of regulatory T cells from the spleen in response to carotid injury. However, deletion of antigen presentation to CD4+ T cells (H20 mice), as well as deletion of regulatory T cells (through treatment with blocking anti-CD25 antibodies), did not affect neointima formation. Also deletion of antigen presentation to CD8+ T cells (Tap10 mice) was without effect on carotid collar-induced neointima formation.ConclusionThe results demonstrate that carotid artery injury is associated with mobilization of regulatory T cells. Depletion of regulatory T cells does not, however, influence the subsequent repair processes leading to the formation of a neointima. The results also demonstrate that lack of CD8+ T cells does not influence neointima formation in presence of functional CD4+ T cells and B cells.
Highlights
Vascular repair responses activated by chronic or acute injury play important roles in the formation of atherosclerotic plaques as well as in plaque healing and development of restenosis after angioplasty [1]
The results demonstrate that carotid artery injury is associated with mobilization of regulatory T cells
Depletion of regulatory T cells does not, influence the subsequent repair processes leading to the formation of a neointima
Summary
Vascular repair responses activated by chronic or acute injury play important roles in the formation of atherosclerotic plaques as well as in plaque healing and development of restenosis after angioplasty [1]. Rag-12/2 mice, which lack mature T and B cells, are characterized by enhanced neointima formation following arterial injury [12] suggesting that adaptive immune responses serves to control the extent of injury-induced repair processes. In accordance with this notion, T cell depletion has been found to result in increased neointima formation following balloon catheter-injury of rat carotid arteries [3] and T cell transfer into Rag-1 mice reduces neointima formation down to similar levels as in wild-type mice [13]. Recent studies by Dimayuga and coworkers demonstrated doi:10.1371/journal.pone.0051556.g001
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
