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The initiation of cell-mediated immunity can be observed as early as the third month of fetal growth, with active antibody-mediated immunity following approximately one month later.
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Bridging Innate and Adaptive Immunity: Understanding and Targeting the Complement System in GVHD Pathogenesis and

Xianhui Wu1, Jiejing Qian1, Hongyan Tong1

  • 1Department of Hematology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China; Zhejiang Provincial Clinical Research Center for Hematological disorders, Hangzhou, China; Zhejiang Key Laboratory for Precision Diagnosis and Treatment of Hematological Maligancies, Hangzhou, China; Zhejiang University Cancer Center, Zhejiang University, Hangzhou, China.

Transplantation and Cellular Therapy
|November 2, 2025
PubMed
Summary
This summary is machine-generated.

Graft-versus-host disease (GVHD) after stem cell transplants poses risks, but the complement system is a new target. Complement-targeted therapies show promise for managing GVHD more effectively and safely.

Keywords:
Allogeneic hematopoietic stem cell transplantationComplement systemGraft-versus-host diseaseTargeted therapy

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Area of Science:

  • Immunology
  • Hematology
  • Transplantation Medicine

Background:

  • Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is curative for high-risk hematological malignancies but limited by graft-versus-host disease (GVHD).
  • Current GVHD treatments (glucocorticoids, immunosuppressants) are insufficient for 30-50% of patients, necessitating novel therapeutic strategies.
  • The complement system, a part of innate immunity, is increasingly recognized as a key player in adaptive immune responses during GVHD.

Purpose of the Study:

  • To review the complement system's role in GVHD pathogenesis.
  • To explore molecular mechanisms linking complement to T/B cell activation and organ damage.
  • To discuss preclinical advances in complement-targeted GVHD therapies.

Main Methods:

  • Literature review focusing on the complement system's involvement in GVHD.
  • Analysis of molecular pathways, including C3a/C5a-C3aR/C5aR signaling.
  • Examination of preclinical data on complement-targeted therapeutic strategies.

Main Results:

  • The complement cascade, particularly C3a/C5a signaling, exacerbates GVHD by promoting Th1/Th17 responses and impairing regulatory T cells (Tregs).
  • Complement components influence T and B cell activation, contributing to target organ damage in GVHD.
  • Preclinical studies demonstrate the potential of complement-targeted therapies for GVHD management.

Conclusions:

  • The complement system is a critical modulator of immune dysregulation in GVHD.
  • Targeting the complement system offers a promising avenue for developing safer and more effective GVHD treatments.
  • Developing complement-directed therapies could lead to personalized GVHD management strategies.