| T cell costimulatory and inhibitory receptors as therapeutic targets for inducing anti-tumor immunity. | |
| | |
MedLine Citation:
|
PMID: 17305478 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Central to the normal function of the immune system is its ability to distinguish between self and non-self since failure to do so could provoke the onset of autoimmune disease. To avoid this possibility, the immune system employs several processes that include, negative selection, peripheral tolerance, and limiting DC antigen priming of naïve T cells to the lymph nodes. Naïve T cells must receive two independent signals from these antigen-presenting cells (APC) that other cells cannot provide if they are to become productively activated. The first is antigen-specific and occurs when T cell antigen receptors encounter the appropriate antigen-MHC complex on the APC--Signal 1. A second, antigen-independent signal is delivered through a T cell costimulatory molecule that engages its APC-expressed ligands--Signal 2. In the absence of a costimulatory signal T cells typically enter a state of anergy. Furthermore, the extent to which T cell activation occurs can be held in check through specific inhibitory receptors expressed on T cells. Understanding the basic mechanisms of how T cell activation is regulated has led to the development of therapeutic approaches for targeting T cell costimulatory and inhibitory pathways for turning on, or preventing the turning off immune responses in subjects with cancer. In this review we will discuss several T cell costimulatory and inhibitory pathways known to influence the development of anti-tumor immunity and how experimental manipulation of these signaling pathways has led to the generation of protective, or curative anti-tumor immunity in mice and humans. |
| | |
Authors:
|
Jeurgen Foell; Becker Hewes; Robert S Mittler |
Related Documents
:
|
22623788 - Arenavirus nucleoproteins prevent activation of nuclear factor kappa b. 22953708 - Moraxella catarrhalis: from interactions with the host immune system to vaccine develop... 19605698 - Functional plasticity of macrophages: in situ reprogramming of tumor-associated macroph... 15748888 - Cell responses to fgfr3 signalling: growth, differentiation and apoptosis. 15463408 - Phagolysosomal escape by intracellular pathogens. 19237318 - Impact of alpha-defensins1-3 on the maturation and differentiation of human monocyte-de... |
Publication Detail:
|
Type: Journal Article; Review |
Journal Detail:
|
Title: Current cancer drug targets Volume: 7 ISSN: 1873-5576 ISO Abbreviation: Curr Cancer Drug Targets Publication Date: 2007 Feb |
Date Detail:
|
Created Date: 2007-02-19 Completed Date: 2007-03-20 Revised Date: 2011-03-30 |
Medline Journal Info:
|
Nlm Unique ID: 101094211 Medline TA: Curr Cancer Drug Targets Country: Netherlands |
Other Details:
|
Languages: eng Pagination: 55-70 Citation Subset: IM |
Affiliation:
|
Department of Pediatrics, Hematology and Oncology and Center for Cell and Gene Therapy, Martin Luther University, Halle-Wittenburg, Germany. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Antigen-Presenting Cells / physiology Antigens, CD / physiology Antigens, CD137 / physiology Antigens, CD28 / physiology* Antigens, CD80 / physiology* Antigens, CD86 / physiology Antigens, Differentiation / physiology Humans Intercellular Signaling Peptides and Proteins / physiology Lymphocyte Activation* Neoplasms / immunology* OX40 Ligand / physiology Signal Transduction T-Lymphocytes / immunology* |
| Chemical | |
Reg. No./Substance:
|
0/Antigens, CD; 0/Antigens, CD137; 0/Antigens, CD28; 0/Antigens, CD80; 0/Antigens, CD86; 0/Antigens, Differentiation; 0/B7-DC antigen; 0/CD274 protein, human; 0/Intercellular Signaling Peptides and Proteins; 0/OX40 Ligand; 0/cytotoxic T-lymphocyte antigen 4 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Cellular and molecular mechanisms of tumor-induced T-cell tolerance.
Next Document: Targeting of Jak/STAT pathway in antigen presenting cells in cancer.