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Costimulation through NKG2D enhances murine CD8+ CTL function: similarities and differences between NKG2D and CD28
Mary A Markiewicz1, Leonidas N Carayannopoulos, Olga V Naidenko
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|August 24, 2005
Summary
NKG2D stimulation costimulates CD8+ T cell responses, enhancing proliferation and cytotoxicity, similar to CD28. However, CD28 is crucial for T cell survival, while NKG2D promotes immune synapse formation without T cell receptor signaling.
Area of Science:
- Immunology
- Cellular Biology
Background:
- NKG2D acts as a costimulatory receptor for CD8+ T cells.
- Recent findings question NKG2D's sufficiency for CD8+ T cell costimulation.
Purpose of the Study:
- Investigate NKG2D's role in CD8+ cytotoxic T lymphocyte (CTL) responses.
- Determine if NKG2D stimulation by RAE1epsilon costimulates effector functions in a specific murine CTL line.
Main Methods:
- Utilized a murine CTL line from DUC18 TCR transgenic mice.
- Stimulated CTLs with P815 cells expressing RAE1epsilon (NKG2D ligand) or B7-1 (CD28 ligand).
- Assessed T cell proliferation, IFN-gamma release, cytotoxicity, Ag-independent cytokine secretion, cell survival, and immune synapse formation.
Main Results:
- NKG2D costimulation enhanced DUC CTL proliferation, IFN-gamma release, and cytotoxicity, mirroring CD28 effects.
- Both RAE1epsilon and B7-1 boosted Ag-independent IFN-gamma secretion.
- CD28 costimulation supported DUC CTL survival during secondary stimulation.
- NKG2D ligation, unlike CD28, induced immune synapse formation without TCR stimulation.
Conclusions:
- NKG2D effectively costimulates CTL effector functions, comparable to CD28.
- Distinct downstream effects of NKG2D and CD28 costimulation exist, impacting T cell survival and synapse formation.
- Further research into these differences will advance understanding of T cell costimulation.