Plasmodium curtails autoimmune nephritis via lasting bone marrow alterations, independent of hemozoin accumulation.

ABSTRACT: The host response against infection with Plasmodium commonly raises self-reactivity as a side effect, and antibody deposition in kidney has been cited as a possible cause of kidney injury during severe malaria. In contrast, animal models show that infection with the parasite confers long-term protection from lethal lupus nephritis initiated by autoantibody deposition in kidney. We have limited knowledge of the factors that make parasite infection more likely to induce kidney damage in humans, or the mechanisms underlying protection from autoimmune nephritis in animal models. Our experiments with the autoimmune-prone FcγR2B[KO] mice have shown that a prior infection with P. yoelii 17XNL protects from end-stage nephritis for a year, even when overall autoreactivity and systemic

SUBMITTER: Amo L 

PROVIDER: S-EPMC10394379 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature