Host immunity to Plasmodium infection: Contribution of Plasmodium berghei to our understanding of T cell-related immune response to blood-stage malaria

Ibraheem, Yarob; Bayarsaikhan, Ganchimeg; Inoue, Shinichi

doi:10.1016/j.parint.2022.102646

Cited by 3 publications

(5 citation statements)

References 96 publications

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“…Host immunity is crucial to inhibit and clear blood-stage Plasmodium infection 11 , specifically splenic germinal center reactions 60 , 61 . Previously, we have shown that gut microbiota composition impacts the severity of malaria via dynamic modulation of spleen germinal center reactions 11 .…”

Section: Discussionmentioning

confidence: 99%

Gut Bacteroides act in a microbial consortium to cause susceptibility to severe malaria

Mandal,

Denny

et al. 2023

Nat Commun

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Malaria is caused by Plasmodium species and remains a significant cause of morbidity and mortality globally. Gut bacteria can influence the severity of malaria, but the contribution of specific bacteria to the risk of severe malaria is unknown. Here, multiomics approaches demonstrate that specific species of Bacteroides are causally linked to the risk of severe malaria. Plasmodium yoelii hyperparasitemia-resistant mice gavaged with murine-isolated Bacteroides fragilis develop P. yoelii hyperparasitemia. Moreover, Bacteroides are significantly more abundant in Ugandan children with severe malarial anemia than with asymptomatic P. falciparum infection. Human isolates of Bacteroides caccae, Bacteroides uniformis, and Bacteroides ovatus were able to cause susceptibility to severe malaria in mice. While monocolonization of germ-free mice with Bacteroides alone is insufficient to cause susceptibility to hyperparasitemia, meta-analysis across multiple studies support a main role for Bacteroides in susceptibility to severe malaria. Approaches that target gut Bacteroides present an opportunity to prevent severe malaria and associated deaths.

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Section: Discussionmentioning

confidence: 99%

Gut Bacteroides act in a microbial consortium to cause susceptibility to severe malaria

Mandal,

Denny

et al. 2023

Nat Commun

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“…Symptomatic disease begins when this blood-stage cycle is repeated. 2,3 Plasmodium parasites target several key organs during their life cycle in human hosts. The liver serves as the starting point for infection as sporozoites multiply in hepatocytes, and one of the most serious complications in malaria involves the brain.…”

Section: Introductionmentioning

confidence: 99%

“…These models are useful for the investigation of malaria in various aspects, including development of antimalarial drugs and vaccines. 3,6 In combination with gene-knockout (KO) mice, the mouse models of malaria have led to uncovering the mechanism underlying T-cell-associated immune response to Plasmodium infection. αβ T cells, such as CD4 + T cells and CD8 + T cells, play a crucial role in the protection against the infection and the infection-associated immunopathology.…”

Section: Introductionmentioning

confidence: 99%

“…The merozoites then replicate and rupture the RBCs. Symptomatic disease begins when this blood‐stage cycle is repeated 2,3 …”

Section: Introductionmentioning

confidence: 99%

“…Mouse models of malaria use rodent‐specific Plasmodium parasites such as P. berghei , P. yoelii , and P. chabaudi . These models are useful for the investigation of malaria in various aspects, including development of antimalarial drugs and vaccines 3,6 . In combination with gene‐knockout (KO) mice, the mouse models of malaria have led to uncovering the mechanism underlying T‐cell–associated immune response to Plasmodium infection.…”

Section: Introductionmentioning

confidence: 99%

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γδ T‐cell–mediated immune responses to malaria

Bayarsaikhan

Ibraheem

Inoue

2023

Microbiology and Immunology

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Malaria is one of the deadliest infectious diseases. Licensed vaccine have demonstrated just over 30% efficacy, and therefore, developing new vaccine candidates and understanding immune responses to Plasmodium have become necessary. γδ T cells have been suggested to be associated with immune responses to malaria due to the observation of their expansion in patients with malaria and experimental models of malaria. γδ T cells act as both “innate‐like” and “adaptive‐like” cells during immune response to malaria. Studies have found that γδ T cells can recognize Plasmodium phosphoantigen, present the antigen, and initiate adaptive immune response during blood‐stage Plasmodium infection. Recent reports also suggested the phagocytic and cytotoxic potential of γδ T cells. Furthermore, γδ T cells can provide protection upon immunization with whole parasite. In addition, γδ T cells during the liver‐stage infection were able to prevent experimental cerebral malaria. Despite these new findings, questions related to γδ T‐cell response during Plasmodium infection remain to be answered. However, investigating these cells in humans remains difficult in many ways; in this regard, rodent models of malarial infection enable us to study these cells in more detail. Insights from experimental malaria models give rise to new cues for development of malarial vaccine and adjunctive therapy for severe malaria. Here, we review our current knowledge of γδ T‐cell immune function in human and experimental mouse malarial infection models; especially, we focus on the mechanisms underlying γδ T cells that are associated with protective immunity during malarial infection.

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γδ T cell-mediated activation of cDC1 orchestrates CD4+ Th1 cell priming in malaria

Ibraheem,

Bayarsaikhan,

Macalinao

et al. 2024

Front. Immunol.

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γδ T cells facilitate the CD4+ T helper 1 (Th1) cell response against Plasmodium infection by activating conventional dendritic cells (cDCs), although the underlying mechanism remains elusive. Our study revealed that γδ T cells promote the complete maturation and production of interleukin-12 and CXCR3-ligands specifically in type 1 cDCs (cDC1), with minimal impact on cDC2 and monocyte derived DCs (Mo-DCs). During the initial infection phase, γδ T cell activation and temporal accumulation in the splenic white pulp, alongside cDC1, occur via CCR7-signaling. Furthermore, cDC1/γδ T cell interactions in the white pulp are amplified through CXCR3 signaling in γδ T cells, optimizing Th1 cell priming by cDC1. We also demonstrated how transitional Th1 cells arise in the white pulp before establishing their presence in the red pulp as fully differentiated Th1 cells. Additionally, we elucidate the reciprocal activation between γδ T cells and cDC1s. These findings suggest that Th1 cell priming is orchestrated by this reciprocal activation in the splenic white pulp during the early phase of blood-stage Plasmodium infection.

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Host immunity to Plasmodium infection: Contribution of Plasmodium berghei to our understanding of T cell-related immune response to blood-stage malaria

Cited by 3 publications

References 96 publications

Gut Bacteroides act in a microbial consortium to cause susceptibility to severe malaria

Gut Bacteroides act in a microbial consortium to cause susceptibility to severe malaria

γδ T‐cell–mediated immune responses to malaria

γδ T cell-mediated activation of cDC1 orchestrates CD4+ Th1 cell priming in malaria

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