The DOI matches its Crossref record; 64 of the 64 references it cites were found in a registry or an index.
Rapamycin-Conditioned Dendritic Cells Are Poor Stimulators of Allogeneic CD4+ T Cells, but Enrich for Antigen-Specific Foxp3+ T Regulatory Cells and Promote Organ Transplant Tolerance
Abstract
The ability of dendritic cells (DC) to regulate Ag-specific immune responses via their influence on T regulatory cells (Treg) may be key to their potential as therapeutic tools or targets for the promotion/restoration of tolerance. In this report, we describe the ability of maturation-resistant, rapamycin (RAPA)-conditioned DC, which are markedly impaired in Foxp3− T cell allostimulatory capacity, to favor the stimulation of murine alloantigen-specific CD4+CD25+Foxp3+ Treg. This was distinct from control DC, especially following CD40 ligation, which potently expanded non-Treg. RAPA-DC-stimulated Treg were superior alloantigen-specific suppressors of T effector responses compared with those stimulated by control DC. Supporting the ability of RAPA to target effector T and B cells, but permit the proliferation and suppressive function of Treg, an infusion of recipient-derived alloantigen-pulsed RAPA-DC followed by a short postoperative course of low-dose RAPA promoted indefinite (>100 day) heart graft survival. This was associated with graft infiltration by CD4+Foxp3+ Treg and the absence of transplant vasculopathy. The adoptive transfer of CD4+ T cells from animals with long-surviving grafts conferred resistance to rejection. These novel findings demonstrate that, whereas maturation resistance does not impair the capacity of RAPA-DC to modulate Treg, it profoundly impairs their ability to expand T effector cells. A demonstration of this mechanism endorses their potential as tolerance-promoting cellular vaccines.
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Cites
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A conditioned dendritic cell can be a temporal bridge between a CD4+ T-helper and a T-killer cell
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Cited by
Regulation of Immune Responses by mTOR
Powell, J. D., Pollizzi, K. N., Heikamp, E. B., & Horton, M. R. (2012) · Annual Review of Immunology · doi:10.1146/annurev-immunol-020711-075024 · Cited by 836
mTOR , metabolism, and the regulation of T‐cell differentiation and function
Waickman, A. T., & Powell, J. D. (2012) · Immunological Reviews · doi:10.1111/j.1600-065x.2012.01152.x · Cited by 420
Roles of mTOR complexes in the kidney: implications for renal disease and transplantation
Fantus, D., Rogers, N. M., Grahammer, F., Huber, T. B., & Thomson, A. W. (2016) · Nature Reviews Nephrology · doi:10.1038/nrneph.2016.108 · Cited by 208
Self-citationXie, L., Sun, F., Wang, J., Mao, X., Xie, L., Yang, S.-H., Su, D.-M., Simpkins, J. W., Greenberg, D. A., & Jin, K. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1303492 · Cited by 175
“It has been reported that rapamycin-treated endothelial cells and dendritic cells may promote Treg activity in ischemic brains (63, 64).”
BackgroundImmune mechanisms in type 1 diabetes
Wållberg, M., & Cooke, A. (2013) · Trends in Immunology · doi:10.1016/j.it.2013.08.005 · Cited by 155
Metadata
- Authors
- Turnquist, H. R., Raimondi, G., Zahorchak, A. F., Fischer, R. T., Wang, Z., & Thomson, A. W.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-06-01
- Volume
- 178
- Issue
- 11
- Pages
- 7018-7031
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1918052238
- Cited by
- 441
- References
- 64
- FWCI
- 11.63
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Rapamycin-Conditioned Dendritic Cells Are Poor Stimulators of Allogeneic CD4+ T Cells, but Enrich for Antigen-Specific Foxp3+ T Regulatory Cells and Promote Organ Transplant Tolerance. https://app.cochat.ai/papers/10.4049/jimmunol.178.11.7018
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- Turnquist, H. R., Raimondi, G., Zahorchak, A. F., Fischer, R. T., Wang, Z., & Thomson, A. W. (2007). Rapamycin-Conditioned Dendritic Cells Are Poor Stimulators of Allogeneic CD4+ T Cells, but Enrich for Antigen-Specific Foxp3+ T Regulatory Cells and Promote Organ Transplant Tolerance. The Journal of Immunology. https://doi.org/10.4049/jimmunol.178.11.7018
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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