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P2Y2 R deletion ameliorates sialadenitis in IL-14α-transgenic mice.

L T Woods1,2, J M Camden1,2, M G Khalafalla1,2

  • 1Department of Biochemistry, University of Missouri, Columbia, MO, USA.

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|January 4, 2018
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Summary
This summary is machine-generated.

The P2Y2 receptor contributes to salivary gland inflammation in a mouse model of Sjögren's syndrome. Blocking this receptor reduced inflammation but did not restore saliva production.

Keywords:
Sjögren's syndromeautoimmunitylymphotoxin-alphanucleotidespurinergic receptorssalivary glands

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Area of Science:

  • Immunology
  • Gastroenterology
  • Rheumatology

Background:

  • Interleukin-14α-transgenic (IL-14αTG) mice exhibit autoimmune exocrinopathy, mimicking Sjögren's syndrome with sialadenitis and hyposalivation.
  • The P2Y2 receptor (P2Y2R) is upregulated during salivary gland inflammation and influences inflammatory responses.

Purpose of the Study:

  • To investigate the role of P2Y2 receptors in autoimmune sialadenitis within the IL-14αTG mouse model.

Main Methods:

  • IL-14αTG mice were crossed with P2Y2R knockout mice (IL-14αTG × P2Y2R-/-).
  • Evaluated P2Y2R expression, lymphocytic infiltration, B- and T-cell accumulation, lymphotoxin-α levels, and saliva secretion in submandibular glands (SMG) at 9 and 12 months.

Main Results:

  • Genetic deletion of P2Y2R significantly reduced B and T lymphocyte infiltration in the SMGs of IL-14αTG mice.
  • Reduced sialadenitis did not restore saliva secretion in the IL-14αTG × P2Y2R-/- mice.
  • Decreased inflammation correlated with reduced lymphotoxin-α levels.

Conclusions:

  • P2Y2 receptors play a role in the development of salivary gland inflammation in IL-14αTG mice.
  • These findings suggest P2Y2R may also contribute to human autoimmune sialadenitis in Sjögren's syndrome.