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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Boomer, Jonathan S. Green, Jonathan M. |
| Description | Country affiliation: United States Author Affiliation: Boomer JS ( Department of Internal Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA.) |
| Abstract | CD28 costimulation regulates a wide range of cellular processes, from proliferation and survival to promoting the differentiation of specialized T-cell subsets. Since first being identified over 20 years ago, CD28 has remained a subject of intense study because of its profound consequences on T cell function and its potential for therapeutic manipulation. In this review we highlight the signaling cascades initiated by the major signaling motifs in CD28, focusing on PI-3 kinase-dependent and -independent pathways and how these are linked to specific cellular outcomes. Recent studies using gene targeted knockin mice have clarified the relative importance of these motifs on in vivo immune responses; however, much remains to be elucidated. Understanding the mechanism behind costimulation holds great potential for development of new clinically relevant reagents, a fact beginning to be realized with the advent of drugs that prevent CD28 ligation and signaling. |
| File Format | HTM / HTML |
| e-ISSN | 19430264 |
| DOI | 10.1101/cshperspect.a002436 |
| Journal | Cold Spring Harbor Perspectives in Biology |
| Issue Number | 8 |
| Volume Number | 2 |
| Language | English |
| Publisher | Cold Spring Harbor Laboratory Press |
| Publisher Date | 2010-08-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Biology Antigens, Cd28 Chemistry T-lymphocytes Metabolism Amino Acid Motifs Animals Cell Line Immune System Lymphocyte Activation Mice Mice, Transgenic Models, Biological Phosphatidylinositol 3-kinases Protein Interaction Mapping Receptors, Antigen, T-cell Signal Transduction Research Support, N.i.h., Extramural |
| Content Type | Text |
| Resource Type | Article |
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