The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
T‐cell costimulatory pathways in allograft rejection and tolerance
Abstract
Summary: The destiny of activated T cells is critical to the ultimate fate of immune response. After encountering antigen, naïve T cells receive signal 1 through the T‐cell receptor (TCR)‐major histocompatibility complex (MHC) plus antigenic peptide complex and signal 2 through ‘positive’ costimulatory molecules leading to full activation. ‘Negative’ T‐cell costimulatory pathways, on the other hand, function to downregulate immune responses. The purpose of this article is to review the current state of knowledge and recent advances in our understanding of the functions of the positive and negative T‐cell costimulatory pathways in alloimmune responses. Specifically, we discuss the functions of the CD28:B7 and the tumor necrosis factor receptor (TNFR):tumor necrosis factor (TNF) family of molecules in allograft rejection and tolerance. We address the following important questions: are T‐cell costimulatory pathways merely redundant or do they provide distinct and unique functions? What are the important and unique interactions between the various pathways? And, what are the effects and mechanisms of targeting of these pathways in different types and patterns of allograft rejection and tolerance models?
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Cites
PD-L2 is a second ligand for PD-1 and inhibits T cell activation
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CD28 and CTLA-4 have opposing effects on the response of T cells to stimulation.
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“Although CD28 is constitutively expressed on T cells, ICOS is induced upon TCR engagement.”
BackgroundInfluentialCTLA-4 is a second receptor for the B cell activation antigen B7.
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“The role of B7-1 versus B7-2 in allograft models Although initial studies in acute rejection models suggested that blockade of both B7-1 and B7-2 is required to prevent rejection and allow long-term engraftment (77–79), subsequent studies support physiological differences.”
BackgroundInfluentialMolecular Basis of T Cell Inactivation by CTLA-4
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Structural Analysis of CTLA-4 Function In Vivo
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“However, association with SHP-2 does not always correlate with CTLA-4 activity and this mechanism remains controversial (6, 55, 62, 66, 67).”
Background
Cited by
Greenwald, R. J., Freeman, G. J., & Sharpe, A. H. (2005) · Annual Review of Immunology · doi:10.1146/annurev.immunol.23.021704.115611 · Cited by 2,318
PD-1 is a regulator of virus-specific CD8+ T cell survival in HIV infection
Petrovas, C., Casazza, J. P., Brenchley, J. M., Price, D. A., Gostick, E., Adams, W. C., Precopio, M. L., Schacker, T., Roederer, M., Douek, D. C., et al. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20061496 · Cited by 889
Physiological and molecular determinants of embryo implantation
Zhang, S., Lin, H., Kong, S., Wang, S., Wang, H., Wang, H., & Armant, D. R. (2013) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2012.12.011 · Cited by 587
Transplantation 50 Years Later — Progress, Challenges, and Promises
Sayegh, M. H., & Carpenter, C. B. (2004) · New England Journal of Medicine · doi:10.1056/nejmon043418 · Cited by 425
Self-citationModulation of T-Cell Activation by Malignant Melanoma Initiating Cells
Schatton, T., Schütte, U., Frank, N. Y., Zhan, Q., Hoerning, A., Robles, S. C., Zhou, J., Hodi, F. S., Spagnoli, G. C., Murphy, G. F., et al. (2010) · Cancer Research · doi:10.1158/0008-5472.can-09-1592 · Cited by 287
Metadata
- Authors
- Rothstein, D. M., & Sayegh, M. H.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2003-11-10
- Volume
- 196
- Issue
- 1
- Pages
- 85-108
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W1966519046
- Cited by
- 222
- References
- 7
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- closed
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- Rothstein, D. M., & Sayegh, M. H. (2003). T‐cell costimulatory pathways in allograft rejection and tolerance. Immunological Reviews. https://doi.org/10.1046/j.1600-065x.2003.00088.x
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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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