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Mice lacking serum amyloid P component do not necessarily develop severe autoimmune disease.

M Soma1, T Tamaoki, H Kawano

  • 1First Department of Biochemistry, Yamanashi Medical University, 1110 Shimokato, Tamaho-cho, Nakakoma-gun, Yamanashi 409-3898, Japan.

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Serum amyloid P component (SAP) deficiency in mice did not cause severe autoimmune disease as previously reported. However, SAP-deficient mice showed resistance to lipopolysaccharide (LPS) toxicity, suggesting a role for SAP in LPS-induced lethality.

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Area of Science:

  • Immunology
  • Pathology

Background:

  • Serum amyloid P component (SAP) is an acute-phase reactant.
  • Previous studies suggested SAP-deficient mice develop autoimmune disease and glomerulonephritis.
  • SAP is known to bind lipopolysaccharide (LPS) and modulate complement activation.

Purpose of the Study:

  • To investigate autoimmune responses in SAP-deficient mice generated in-house.
  • To determine the role of SAP in LPS-induced toxicity.

Main Methods:

  • Generated and phenotypically analyzed SAP-deficient mice.
  • Assessed autoantibody production and glomerulonephritis development.
  • Administered Salmonella typhimirium LPS intraperitoneally to assess survival.

Main Results:

  • SAP-deficient mice produced anti-nuclear antibodies but did not develop severe glomerulonephritis.
  • SAP-deficient mice exhibited resistance to lethal effects of high-dose LPS.
  • Findings contradict previous reports on SAP deficiency-induced autoimmune disease.

Conclusions:

  • SAP deficiency does not appear to cause severe autoimmune disease in mice.
  • SAP plays a critical role in the toxicity of LPS.
  • Further research is warranted to elucidate SAP's role in immune responses and LPS toxicity.