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Balancing in a black box: Potential immunomodulatory roles for TGF-β signaling during blood-stage malaria.

Authors
  • Drewry, Lisa L1
  • Harty, John T1, 2, 3
  • 1 Department of Microbiology and Immunology, University of Iowa, Iowa City, IA, USA.
  • 2 Department of Pathology, University of Iowa, Iowa City, IA, USA.
  • 3 Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA, USA.
Type
Published Article
Journal
Virulence
Publisher
Landes Bioscience
Publication Date
Dec 01, 2020
Volume
11
Issue
1
Pages
159–169
Identifiers
DOI: 10.1080/21505594.2020.1726569
PMID: 32043415
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Malarial disease caused by Plasmodium parasites challenges the mammalian immune system with a delicate balancing act. Robust inflammatory responses are required to control parasite replication within red blood cells, which if unchecked, can lead to severe anemia and fatality. However, the same inflammatory response that controls parasite replication is also associated with immunopathology and severe disease, as is exemplified by cerebral malaria. A robust literature has identified critical roles for innate, cellular, and humoral immune responses orchestrated by IFN-γ and TH1 type responses in controlling blood stage malarial disease. In contrast, TGF-β and IL-10 have been identified as important anti-inflammatory immunomodulators that help to limit inflammation and pathology during malaria. TGF-β is a pleiotropic cytokine, with the ability to exert a wide variety of context-dependent immunomodulatory roles.The specific mechanisms that allow TGF-β to protect against malarial pathology remain essentially unexplored and offer a promising avenue to dissect the most critical elements of immunomodulation in avoiding severe malaria. Here we discuss potential immunomodulatory roles for TGF-β during malaria in light of recent advances in our understanding of the role of Tregs during blood-stage malaria.

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