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Age-dependent decrease of polymeric Ig receptor expression and IgA elevation in ddY mice: a possible cause of IgA

Takeshi Yanagihara1, Yoshihiro Kumagai, Yoshihiko Norose

  • 1Department of Microbiology and Immunology, Nippon Medical School, Tokyo, Japan.

Laboratory Investigation; a Journal of Technical Methods and Pathology
|November 25, 2003
PubMed
Summary

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A defect in polymeric Ig receptors (pIgRs) impairs IgA clearance, leading to elevated serum IgA and IgA nephropathy (IgAN)-like symptoms in aging ddY mice.

Area of Science:

  • Immunology
  • Nephrology
  • Animal Models

Background:

  • Age-dependent elevation of serum IgA and IgA nephropathy (IgAN)-like symptoms are observed in ddY mice.
  • Understanding the underlying mechanisms is crucial for human IgAN research.

Purpose of the Study:

  • To investigate the cause of elevated serum IgA and IgAN-like symptoms in aging ddY mice.
  • To identify the role of polymeric Ig receptors (pIgRs) in IgA homeostasis and disease pathogenesis.

Main Methods:

  • Classification of ddY mice into high and normal serum IgA subgroups.
  • Analysis of urinary IgA to serum IgA ratio and IgA clearance rates.
  • Assessment of pIgR expression in glomeruli and intestine using polymerase chain reaction (PCR).

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Main Results:

  • ddY(High) mice exhibited reduced urinary IgA/serum IgA ratio and slower IgA clearance.
  • Poor expression of pIgRs was observed in the glomeruli and intestine of ddY(High) mice.
  • Decreased pIgR expression in ddY(High) mice was confirmed at the transcriptional level.

Conclusions:

  • Systemic defect in pIgR expression leads to impaired IgA secretion and serum IgA accumulation.
  • Age-dependent changes in pIgR expression contribute to elevated serum IgA and IgAN pathogenesis.
  • ddY mice serve as a valuable model for studying IgAN and IgA-related disorders.