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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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Related Experiment Video

Updated: Jun 12, 2025

Overlapping Peptide Library to Map Qa-1 Epitopes in a Protein
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C1q reprograms innate immune memory.

Inge Jonkman1, Maaike M E Jacobs1, Yutaka Negishi2,3

  • 1Department of Nephrology, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Netherlands.

Frontiers in Immunology
|June 9, 2025
PubMed
Summary
This summary is machine-generated.

Complement component 1q (C1q) suppresses innate immune memory by reprogramming myeloid cell metabolism and gene expression. This discovery reveals a link between the complement system and trained immunity, impacting host defense and disease.

Keywords:
C1qcomplementimmunometabolisminnate immune memorytolerancetrained immunity

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Area of Science:

  • Immunology
  • Molecular Biology
  • Metabolic Regulation

Background:

  • Trained immunity, a form of innate immune memory, involves metabolic and epigenetic reprogramming of immune cells.
  • This process influences host defense and immune-mediated diseases.
  • The role of the complement system in trained immunity remains largely unexplored.

Purpose of the Study:

  • To investigate the role of complement component 1q (C1q) in modulating innate immune memory.
  • To elucidate the molecular mechanisms by which C1q affects myeloid cell responsiveness and metabolism.

Main Methods:

  • Analysis of C1q's effect on myeloid cell metabolism, focusing on glycolysis.
  • Examination of C1q's impact on the transcriptional regulation of inflammatory and metabolic genes.
  • Correlation of genetic variations near the C1q gene with trained immunity induction.

Main Results:

  • C1q was identified as a potent suppressor of innate immune memory in myeloid cells.
  • C1q induces significant metabolic reprogramming, particularly in glycolysis.
  • C1q controls the expression of key metabolic and inflammatory genes.
  • Genetic variations near C1q associate with trained immunity induction by BCG and beta-glucan.

Conclusions:

  • C1q acts as a key immunomodulator of innate immune memory.
  • A molecular link exists between the complement system and trained immunity.
  • These findings enhance the understanding of innate immune memory regulation and its implications.