A Protective and Pathogenic Role for Complement During Acute Toxoplasma gondii Infection
Patricia M Sikorski1,2, Alessandra G Commodaro1, Michael E Grigg1
1Molecular Parasitology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
Frontiers in Cellular and Infection Microbiology
|March 11, 2021
Summary
Toxoplasma gondii evades host complement killing by recruiting regulatory proteins. This strategy balances parasite survival with immune responses, controlling infection and promoting transmission.
Area of Science:
- Immunology
- Parasitology
- Molecular Biology
Background:
- Toxoplasma gondii infection relies on evading the host complement system.
- The parasite recruits host complement regulatory proteins to its surface, inhibiting lysis.
Purpose of the Study:
- To review how Toxoplasma gondii manipulates the complement system for infection.
- To understand the dual role of complement regulation in controlling parasite burden and immune responses.
Main Methods:
- Literature review of studies on Toxoplasma gondii and complement interaction.
- Analysis of complement regulatory mechanisms employed by the parasite.
Main Results:
- Toxoplasma gondii recruits C4BP and Factor H (FH) to inhibit C3 and MAC formation.
- Complement inactivation protects against lysis but allows C3 split products to mediate opsonization and immunomodulation.
- Complement regulation controls systemic parasite burden but exacerbates local gut immunity in susceptible mice.
Conclusions:
- Toxoplasma gondii balances complement inactivation for survival with generating immune signals for protective immunity.
- This intricate regulation promotes parasite persistence, host survival, and transmission.
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