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γδT-cell function in sepsis is modulated by C5a receptor signalling
Gencheng Han1, Shaoxia Geng, Yurong Li
1Department of Molecular Immunology, Institute of Basic Medical Sciences, Beijing, China. genchenghan@yahoo.com
Immunology
|April 20, 2011
Summary
Gamma delta T cells express the complement C5a receptor (C5aR, CD88), which is upregulated during sepsis. C5aR activation on these cells enhances interleukin-17 (IL-17) production via the PI3K/Akt pathway.
Area of Science:
- Immunology
- Cellular Biology
- Sepsis Pathogenesis
Background:
- Gamma delta T (γδT) cells are implicated in sepsis pathogenesis.
- The precise mechanisms governing γδT cell involvement in sepsis remain incompletely understood.
Purpose of the Study:
- To investigate the expression and function of the complement C5a receptor (C5aR, CD88) on γδT cells during sepsis.
- To elucidate the signaling pathways involved in C5aR-mediated γδT cell activation and function.
Main Methods:
- Analysis of C5aR (CD88) expression on γδT cells in septic mice at protein and mRNA levels.
- In vivo C5a neutralization experiments.
- In vitro incubation of γδT cells with recombinant C5a.
- Assessment of IL-17 production and PI3K/Akt pathway activation.
Main Results:
- γδT cells express C5aR (CD88), with expression upregulated in sepsis.
- C5aR expression is regulated by complement C5a, both in vivo and in vitro.
- C5aR ligation on γδT cells promotes IL-17 secretion.
- Activation of the PI3K/Akt signaling pathway by C5aR ligation enhances γδT cell function.
Conclusions:
- C5a directly acts on C5aR expressed by γδT cells, leading to cell activation.
- This interaction enhances IL-17 production capacity of γδT cells.
- The PI3K/Akt pathway is crucial for C5a-mediated upregulation of γδT cell function in sepsis.
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