Both LTβ Receptor and TNF Receptor 2 Are Needed for Experimental Cerebral Malaria Development
Author Information
Author(s): Togbe Dieudonnée, Loureiro de Sousa Paulo, Fauconnier Mathilde, Boissay Victorine, Fick Lizette, Scheu Stefanie, Pfeffer Klaus, Menard Robert, Grau Georges E., Doan Bich-Thuy, Beloeil Jean Claude, Renia Laurent, Hansen Anna M., Ball Helen J., Hunt Nicholas H., Ryffel Bernhard, Quesniaux Valerie F. J.
Primary Institution: University of Orléans and CNRS, Molecular Immunology and Embryology UMR6218, Orleans, France
Hypothesis
Are both LTβR and TNFR2 signaling necessary for the development of experimental cerebral malaria?
Conclusion
Both LTβR and TNFR2 signaling are essential for developing microvascular pathology that leads to fatal experimental cerebral malaria.
Supporting Evidence
- LTβR deficient mice did not develop neurological signs of cerebral malaria.
- Wild-type mice developed distinct microvascular pathology.
- Absence of LTβR signaling prevented microvascular lesions in the brain.
- Magnetic resonance imaging showed normal cerebral perfusion in LTβR deficient mice.
- LTβR deficient mice had significantly lower recruitment of CD8+ T cells in the brain.
Takeaway
This study found that two specific receptors in the immune system are important for developing a severe form of malaria in mice, and without them, the mice do not get sick.
Methodology
The study used LTβR deficient mice and various imaging techniques to assess the development of cerebral malaria and the associated microvascular pathology.
Limitations
The study was conducted in mice, which may not fully replicate human disease.
Participant Demographics
Mice used were of the C57BL/6 genetic background.
Statistical Information
P-Value
<0.0001
Statistical Significance
p<0.0001
Digital Object Identifier (DOI)
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