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SOD3 suppresses early cellular immune responses to parasite infection

Author

Listed:
  • Qilong Li

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Kunying Lv

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Ning Jiang

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Tong Liu

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Nan Hou

    (Chinese Academy of Medical Sciences & Peking Union Medical College)

  • Liying Yu

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Yixin Yang

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Anni Feng

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Yiwei Zhang

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Ziwei Su

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Xiaoyu Sang

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Ying Feng

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Ran Chen

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

  • Wenyue Xu

    (Army Medical University (Third Military Medical University))

  • Liwang Cui

    (University of South Florida)

  • Yaming Cao

    (China Medical University)

  • Qijun Chen

    (Shenyang Agricultural University
    Chinese Academy of Medical Sciences)

Abstract

Host immune responses are tightly controlled by various immune factors during infection, and protozoan parasites also manipulate the immune system to evade surveillance, leading to an evolutionary arms race in host‒pathogen interactions; however, the underlying mechanisms are not fully understood. We observed that the level of superoxide dismutase 3 (SOD3) was significantly elevated in both Plasmodium falciparum malaria patients and mice infected with four parasite species. SOD3-deficient mice had a substantially longer survival time and lower parasitemia than control mice after infection, whereas SOD3-overexpressing mice were much more vulnerable to parasite infection. We revealed that SOD3, secreted from activated neutrophils, bound to T cells, suppressed the interleukin-2 expression and concomitant interferon-gamma responses crucial for parasite clearance. Overall, our findings expose active fronts in the arms race between the parasites and host immune system and provide insights into the roles of SOD3 in shaping host innate immune responses to parasite infection.

Suggested Citation

  • Qilong Li & Kunying Lv & Ning Jiang & Tong Liu & Nan Hou & Liying Yu & Yixin Yang & Anni Feng & Yiwei Zhang & Ziwei Su & Xiaoyu Sang & Ying Feng & Ran Chen & Wenyue Xu & Liwang Cui & Yaming Cao & Qiju, 2024. "SOD3 suppresses early cellular immune responses to parasite infection," Nature Communications, Nature, vol. 15(1), pages 1-10, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-49348-0
    DOI: 10.1038/s41467-024-49348-0
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    References listed on IDEAS

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