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Related Concept Videos

Malaria01:29

Malaria

Malaria pathogenesis in humans reflects a delicate interplay between parasite biology and host response. Clinical illness reflects a host’s immune response to the parasite’s asexual replication cycle, which is often asymptomatic in individuals with partial immunity. From the parasite's perspective, transmission between mosquito and human with minimal host pathology is evolutionarily advantageous. Among the six Plasmodium species infecting humans, P. falciparum and P. vivax dominate in global...
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

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Related Experiment Video

Updated: Jul 12, 2026

Myeloid Cell Isolation from Mouse Skin and Draining Lymph Node Following Intradermal Immunization with Live Attenuated Plasmodium Sporozoites
08:46

Myeloid Cell Isolation from Mouse Skin and Draining Lymph Node Following Intradermal Immunization with Live Attenuated Plasmodium Sporozoites

Published on: May 18, 2016

Systemic tumor necrosis factor generated during lethal Plasmodium infections impairs dendritic cell function.

Michelle N Wykes1, Xue Q Liu, Suhua Jiang

  • 1The Molecular Immunology Laboratory, The Queensland Institute of Medical Research, The Bancroft Centre, Brisbane, Queensland, Australia.

Journal of Immunology (Baltimore, Md. : 1950)
|September 6, 2007
PubMed
Summary

Tumor necrosis factor-alpha (TNF-α) impairs dendritic cell (DC) function during lethal malaria infections. Blocking TNF-α restores DC activity, suggesting a key role in malaria-induced immunosuppression.

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Myeloid Cell Isolation from Mouse Skin and Draining Lymph Node Following Intradermal Immunization with Live Attenuated Plasmodium Sporozoites
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Fluorescence-activated Cell Sorting for Purification of Plasmacytoid Dendritic Cells from the Mouse Bone Marrow

Published on: November 4, 2016

Area of Science:

  • Immunology
  • Parasitology
  • Infectious Diseases

Background:

  • Dendritic cells (DCs) are crucial for initiating immune responses, including those against malaria parasites.
  • Previous studies present conflicting findings on DC function during malaria infection, with some reporting normal function and others compromised function.

Purpose of the Study:

  • To investigate the reasons for differing findings on DC function during malaria.
  • To determine the impact of different Plasmodium species (lethal vs. non-lethal) on DC function.
  • To elucidate the role of Tumor Necrosis Factor-alpha (TNF-α) in malaria-associated DC dysfunction.

Main Methods:

  • Mice were infected with lethal (Plasmodium berghei, P. vinckei) or non-lethal (P. yoelii 17XNL, P. chabaudi) malaria parasites.
  • Dendritic cell phenotype, endocytosis, IL-12 secretion, and antigen presentation were assessed.
  • Experiments were conducted using TNF-α knockout (TNF-KO) mice to evaluate the cytokine's role.

Main Results:

  • DCs from mice infected with lethal malaria species showed uniform maturation and functional impairment (reduced endocytosis, IL-12 secretion, and T cell presentation) 7 days post-infection.
  • These DC impairments correlated with peak systemic TNF-α levels during lethal infections.
  • In TNF-KO mice, DC phenotype, antigen presentation, and IL-12 secretion remained normal even after lethal malaria infections.

Conclusions:

  • Systemic production of TNF-α significantly contributes to the impaired function of dendritic cells during lethal malaria infections.
  • These findings offer a partial explanation for the immunosuppression observed in malaria.
  • Targeting TNF-α may be a therapeutic strategy to restore immune function during severe malaria.