Parasites exploit the binding of host SOD3 to T cells, resulting in the impairment of T cells’ ability to defend against pathogen infection. The Monkey King is indicative of cytotoxic T cells Golden Cloth Rope is indicative of host SOD3 Monster is indicative of parasites Golden cudgel is indicative of immune effective factors such as IFN-γ. Parasites hijack host T cells via elevated expression of SOD3, resulted in the impairment of early immune reaction against parasite infection.
New research reveals how a protein called superoxide dismutase 3 plays a surprising role in weakening the body’s defense system during parasitic infections. A team of scientists, led by Dr. Qijun Chen from Shenyang Agricultural University in China, to uncover these findings, which are published in the journal Nature Communications.
Researchers explored how the immune system, which protects the body against harmful invaders, responds to parasitic infections, focusing on the role of superoxide dismutase 3. This protein, which usually helps reduce harmful molecules called reactive oxygen species (damaging molecules produced during infections), is manipulated by parasites to avoid being destroyed. The study found that patients with malaria and mice infected with certain parasites had higher levels of this protein in their bodies. Remarkably, mice that did not produce superoxide dismutase 3 survived longer and had fewer parasites in their blood compared to normal mice. This suggests the protein might help parasites survive by interfering with the body’s natural defenses.
The scientists discovered that superoxide dismutase 3 is released by a type of white blood cell called neutrophils, which are immune cells that respond early to infections. This protein attaches to a different kind of immune cell, known as T cells, which are crucial for coordinating the body’s attack on infections, and prevents them from producing important molecules that signal the body to fight the infection. One of these molecules is interleukin-2, a type of protein that helps activate immune responses, while the other is interferon-gamma, which is essential for clearing parasites from the body. “Our findings expose active fronts in the arms race between parasites and the host immune system,” Dr. Chen explained, emphasizing the struggle between the body’s defenses and the parasites’ survival strategies.
Scientists also showed that mice lacking superoxide dismutase 3 produced more interferon-gamma early in the infection, which strengthened their ability to fight off parasites like Plasmodium (the parasite responsible for malaria) and Toxoplasma gondii (a parasite that can cause serious complications in humans and animals). In contrast, animals with higher levels of the protein were more vulnerable to these infections. The researchers explained that while superoxide dismutase 3 normally helps protect the body from harmful molecules, its involvement in weakening the immune response can make it easier for parasites to thrive.
Therapies targeting superoxide dismutase 3 could offer new ways to treat parasitic infections. For example, blocking this protein’s activity might strengthen the body’s defenses and make it harder for parasites to survive. “Superoxide dismutase 3 could serve as a potential target for developing interventions to reduce the severity of diseases caused by protozoan parasites,” said Dr. Chen. However, they also noted that more research is needed to fully understand how this protein works and to develop effective treatments.
These findings highlight a surprising way parasites exploit the body’s immune system, opening new possibilities for research into therapies that could better prepare the body to combat these infections.
Journal Reference
Li, Q., Lv, K., Jiang, N., et al. “SOD3 suppresses early cellular immune responses to parasite infection.” Nature Communications, 2024. DOI: https://doi.org/10.1038/s41467-024-49348-0
About the Author
Dr Qijun Chen, a prominent parasitologist, has been working on protozoan parasites and associated diseases for more than 30 years. He started his high education at the Changchun Veterinary University in 1981 and obtained a Ph.D. degree in 1994. He had his postdoc training in Mats Wahlgren’s group at the Karolinska Institute (KI) in Stockholm, Sweden. His research career started immediately afterwards with tenure-track positions as an Associated Professor at the KI and a senior research scientist at the Swedish Institute for Infectious Disease Control. He has been focused on the parasite pathogenicity of Plasmodium falciparum with an aim of understanding the molecular background of severe malaria pathogenesis. From then, he has been actively working at the forefront of research on malaria with outstanding discoveries in parasite biology and host-parasite interactions with an extensive track record and well-recognized publications. He was appointed as the chief parasitologist of Jilin University (China) and the Chinese Academy of Medical Sciences in 2006, and continued his study on protozoan parasites including Plasmodium species, Toxoplasma gondii and Trypanosoma brucei. From 2018 to 2024, he served as the president of Shenyang Agricultural University. Now he is the leading scientist of the National Key Research and Development Plan Project, which is a consortium of basic research on protozoan parasites, spanning from 2016 to 2025. Dr. Q. Chen has made great contributions in understanding the genetic, epigenetic regulation and functional biology of the protozoan parasites in the context of host-parasite interaction. He has published more than 160 articles and invited reviews with high citation records.
