Background: Malaria, caused by Plasmodium sp. parasites, is a leading cause of global morbidity and mortality. Cerebral malaria, characterized by neurological symptoms, is a life-threatening complication of malaria affecting over 500,000 young children in Africa every year. Because of the prevalence and severity of cerebral malaria, a better understanding of the underlying molecular mechanisms of its pathology is desirable and could inform future development of therapeutics. This study sought to clarify the role of Toll-like receptors (TLRs) in promoting immunopathology associated with cerebral malaria, with a particular focus on the understudied TLR7. Methods. Using the Plasmodium berghei ANKA mouse model of experimental cerebral malaria, C57BL/6 mice deficient in various TLRs were infected, and their resistance to cerebral malaria and immune activation through cytokine production were measured. Results: Loss of TLR7 conferred partial protection against fatal experimental cerebral malaria. Additionally, loss of TLR signalling dysregulated the cytokine profile, resulting in a shift in the cytokine balance towards those with more anti-inflammatory properties. Conclusion: This work identifies signalling through TLR7 as a source of pathology in experimental cerebral malaria.
CITATION STYLE
Baccarella, A., Huang, B. W., Fontana, M. F., & Kim, C. C. (2014). Loss of Toll-like receptor 7 alters cytokine production and protects against experimental cerebral malaria. Malaria Journal, 13(1). https://doi.org/10.1186/1475-2875-13-354
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