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Cognate antigen stimulation generates potent CD8(+) inflammatory effector T cells.
Hsueh-Cheng Sung1, Sara Lemos1, Patricia Ribeiro-Santos1
1Faculté de Médecine, U1020, Université Paris-Descartes, INSERM , Paris , France.
Frontiers in Immunology
|January 1, 2014
Summary
Inflammation typically starts with innate immunity. However, this study reveals that CD8 T cells can initiate inflammatory reactions by releasing cytokines and chemokines, even without prior inflammation.
Area of Science:
- Immunology
- Cellular Biology
Background:
- Inflammatory reactions are crucial for immunity, traditionally initiated by innate signals.
- Lymphocyte involvement, like T helper 17 (TH17) cells, typically requires a pre-existing inflammatory environment.
Purpose of the Study:
- To investigate the role of CD8 T cells in initiating inflammatory reactions.
- To challenge the conventional view of inflammation originating solely from innate immunity.
Main Methods:
- Utilized sterile immunizations and MyD88-deficient mouse models.
- Analyzed cytokine and chemokine production by CD8 T cells.
- Quantified cell mobilization following CD8 T cell activation.
Main Results:
- CD8 T cells, even in sterile or MyD88-deficient conditions, rapidly produce pro-inflammatory cytokines and chemokines.
- These inflammatory functions precede CD8 T cell expansion and wane before antigen clearance.
- A small number of CD8 T cells can mobilize a large population of immune cells.
Conclusions:
- CD8 T cell responses can initiate local inflammatory reactions, independent of traditional innate immune triggers.
- This finding redefines the initiation phase of inflammation and the role of CD8 T cells within it.
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