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Collectin11 and Complement Activation in IgA Nephropathy.

Min Wei1,2,3,4,5, Wei-Yi Guo1,2,3,4,5, Bo-Yang Xu1,2,3,4,5

  • 1Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China.

Clinical Journal of the American Society of Nephrology : CJASN
|October 7, 2021
PubMed
Summary
This summary is machine-generated.

Collectin11, a complement pathway initiator, is found in IgA nephropathy kidneys. It activates complement and contributes to kidney injury in some patients.

Keywords:
IgA nephropathycollectinscomplementcomplement activationmesangial cells

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Area of Science:

  • Nephrology
  • Immunology
  • Complement System

Background:

  • IgA nephropathy (IgAN) is the most common primary glomerulonephritis globally.
  • Collectin11, a complement lectin pathway initiator, is implicated in acute kidney injury and tubulointerstitial fibrosis.
  • The role of collectin11 in IgAN pathogenesis requires further investigation.

Purpose of the Study:

  • To investigate the role of collectin11 in the pathogenesis of IgA nephropathy.
  • To examine collectin11 deposition and its interaction with IgA1 in IgAN glomeruli.
  • To elucidate the functional consequences of collectin11 in IgAN mesangial cells.

Main Methods:

  • Immunofluorescence to detect collectin11 and complement protein deposition in kidney biopsies.
  • In vitro studies using human mesangial cells treated with IgA1 immune complexes.
  • Quantitative RT-PCR and immunofluorescence to assess collectin11 expression.
  • Proximity ligation assays to confirm codeposition.

Main Results:

  • Collectin11 codeposition with IgA1 was observed in 37% of IgAN participants.
  • IgA1 immune complexes stimulated collectin11 secretion and cell surface deposition.
  • Collectin11 bound to IgA1 immune complexes and initiated complement activation, accelerating C3 deposition.

Conclusions:

  • Collectin11, produced by mesangial cells, plays a role in IgAN kidney injury.
  • Collectin11-induced complement activation contributes to the pathogenesis of IgAN.
  • This highlights a potential therapeutic target in a subset of IgAN patients.