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Updated: Jul 19, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Anthrax toxins inhibit immune cell chemotaxis by perturbing chemokine receptor signalling
Silvia Rossi Paccani1, Fiorella Tonello, Laura Patrussi
1Department of Evolutionary Biology, University of Siena, Via Aldo Moro 2, 53100 Siena, Italy.
Abstract:
Pathogenic strains of Bacillus anthracis produce two potent toxins, lethal toxin (LT), a metalloprotease that cleaves mitogen-activated protein kinase kinases, and oedema toxin (ET), a calcium/calmodulin-dependent adenylate cyclase. Emerging evidence indicates a role for both toxins in suppressing the initiation of both innate and adaptive immune responses, which are essential to keep the infection under control. Here we show that LT and ET inhibit chemotaxis of T-cells and macrophages by subverting signalling by both CXC and CC chemokine receptors. The data highlight a novel strategy of immunosuppression by B. anthracis based on inhibition of immune cell homing.
Insights
Bacillus anthracis toxins, lethal toxin (LT) and oedema toxin (ET), suppress immune responses by inhibiting T-cell and macrophage movement. This novel immunosuppression strategy hinders immune cell homing, crucial for controlling infection.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Bacillus anthracis produces lethal toxin (LT) and oedema toxin (ET).
- Both toxins are implicated in suppressing innate and adaptive immune responses.
- Immune cell chemotaxis is essential for controlling infections.
Purpose of the Study:
- To investigate the role of LT and ET in immune cell chemotaxis.
- To elucidate the mechanism by which B. anthracis suppresses immune responses.
Main Methods:
- Studied the effects of LT and ET on T-cell and macrophage chemotaxis.
- Investigated the involvement of CXC and CC chemokine receptors in toxin-mediated inhibition.
Main Results:
- LT and ET were found to inhibit the chemotaxis of T-cells and macrophages.
- This inhibition was mediated by subverting signaling pathways of CXC and CC chemokine receptors.
- B. anthracis employs a novel immunosuppression strategy by blocking immune cell homing.
Conclusions:
- Bacillus anthracis utilizes LT and ET to inhibit immune cell homing.
- This mechanism represents a novel strategy for immune evasion by B. anthracis.
- Understanding this pathway is crucial for developing countermeasures against anthrax.
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