In:
Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-9-30)
Abstract:
Cerebral malaria is a potentially lethal disease, which is caused by excessive inflammatory responses to Plasmodium parasites. Here we use a newly developed transgenic Plasmodium berghei ANKA ( PbA Ama1 OVA ) parasite that can be used to study parasite-specific T cell responses. Our present study demonstrates that Ifnar1 -/- mice, which lack type I interferon receptor-dependent signaling, are protected from experimental cerebral malaria (ECM) when infected with this novel parasite. Although CD8 + T cell responses generated in the spleen are essential for the development of ECM, we measured comparable parasite-specific cytotoxic T cell responses in ECM-protected Ifnar1 -/- mice and wild type mice suffering from ECM. Importantly, CD8 + T cells were increased in the spleens of ECM-protected Ifnar1 -/- mice and the blood-brain-barrier remained intact. This was associated with elevated splenic levels of CCL5, a T cell and eosinophil chemotactic chemokine, which was mainly produced by eosinophils, and an increase in eosinophil numbers. Depletion of eosinophils enhanced CD8 + T cell infiltration into the brain and increased ECM induction in PbA Ama1 OVA -infected Ifnar1 -/- mice. However, eosinophil-depletion did not reduce the CD8 + T cell population in the spleen or reduce splenic CCL5 concentrations. Our study demonstrates that eosinophils impact CD8 + T cell migration and proliferation during PbA Ama1 OVA -infection in Ifnar1 -/- mice and thereby are contributing to the protection from ECM.
Type of Medium:
Online Resource
ISSN:
1664-3224
DOI:
10.3389/fimmu.2021.711876
DOI:
10.3389/fimmu.2021.711876.s001
DOI:
10.3389/fimmu.2021.711876.s002
DOI:
10.3389/fimmu.2021.711876.s003
DOI:
10.3389/fimmu.2021.711876.s004
DOI:
10.3389/fimmu.2021.711876.s005
DOI:
10.3389/fimmu.2021.711876.s006
DOI:
10.3389/fimmu.2021.711876.s007
DOI:
10.3389/fimmu.2021.711876.s008
DOI:
10.3389/fimmu.2021.711876.s009
DOI:
10.3389/fimmu.2021.711876.s010
Language:
Unknown
Publisher:
Frontiers Media SA
Publication Date:
2021
detail.hit.zdb_id:
2606827-8
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