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Imaging the Human Immunological Synapse
Published on: December 26, 2019
IL-12 enhances CTL synapse formation and induces self-reactivity
Mary A Markiewicz1, Erica L Wise, Zachary S Buchwald
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|January 22, 2009
Summary
Cytokines impact T cell synapse formation. Interleukin-12 (IL-12) enhances synapse formation and T cell responsiveness to weak peptides, while TGF-beta decreases it, with implications for T cell-mediated autoimmunity.
Area of Science:
- Immunology
- Cellular Biology
- Molecular Medicine
Background:
- Immunological synapse formation is crucial for T cell receptor (TCR) signaling outcomes.
- The role of factors beyond TCR signaling in synapse formation efficiency remains unclear.
Purpose of the Study:
- To investigate the influence of cytokines on the formation of immunological synapses between murine cytotoxic T lymphocytes (CTLs) and target cells.
- To determine the functional consequences of cytokine-modulated synapse formation.
Main Methods:
- Murine CTLs and target cells were treated with cytokines.
- Immunological synapse formation was assessed.
- T cell responses to varying peptide strengths, including self-peptides, were measured.
- LFA-1 avidity was analyzed on treated CTLs.
Main Results:
- Interleukin-12 (IL-12) significantly enhanced CTL-target cell synapse formation.
- Transforming growth factor-beta (TGF-beta) decreased synapse formation.
- IL-12 treatment enabled T cells to respond to weak and self-peptides, indicating enhanced functional avidity.
- Enhanced synapse formation correlated with increased functional avidity of LFA-1.
Conclusions:
- Cytokines, specifically IL-12 and TGF-beta, modulate immunological synapse formation.
- IL-12 enhances T cell function by increasing synapse formation and LFA-1 avidity, enabling responses to previously unresponsive antigens.
- These findings suggest a significant role for IL-12 in T cell-mediated autoimmunity.
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