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CD166 expression, characterization, and localization in salivary epithelium: implications for function during

Syed M A Abidi1, Mohammad K Saifullah, Marie D Zafiropulos

  • 1Department of Pediatrics, CASE School of Medicine and Rainbow Babies and Children's Hospital, Cleveland, Ohio 44106, USA.

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Summary

In Sjögren's syndrome, CD166 (a cell adhesion molecule) gains function in salivary glands, increasing its association with the cytoskeleton and binding to CD6, potentially driving inflammation.

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Area of Science:

  • Immunology
  • Cell Biology
  • Rheumatology

Background:

  • CD166, an immunoglobulin superfamily molecule, interacts with CD6 and is implicated in immune responses.
  • CD166 is upregulated in certain cancers and rheumatoid arthritis.
  • CD166 expression in salivary epithelium prompted investigation into its role in Sjögren's syndrome.

Purpose of the Study:

  • To investigate the function and expression of CD166 and CD6 in mouse salivary glands during sialoadenitis, a model for Sjögren's syndrome.
  • To determine if CD166 expression correlates with its function in salivary epithelium.
  • To elucidate the molecular mechanisms underlying CD166 involvement in salivary gland inflammation.

Main Methods:

  • Utilized recombinant soluble CD6-Ig to assess binding to salivary epithelial cells.
  • Performed cross-blocking studies to identify CD166 as a CD6 ligand.
  • Employed anti-CD166 antibodies and CD6-Ig for immunoprecipitation.
  • Analyzed CD166 colocalization with the actin cytoskeleton in sialoadenitis models.

Main Results:

  • CD6-Ig bound to CD6 ligands on salivary epithelial cells, with binding partially dependent on CD166.
  • CD166 was detected in salivary epithelium, but its expression did not always predict function.
  • IFN-gamma treatment enhanced CD166 precipitation by CD6-Ig, and increased CD166 colocalization with the actin cytoskeleton in inflamed salivary glands.

Conclusions:

  • During sialoadenitis, CD166 exhibits a gain of function, associating more closely with the actin cytoskeleton.
  • This altered CD166 function leads to increased binding capacity with CD6.
  • Dysregulated CD166 function may contribute to the inflammatory processes observed in Sjögren's syndrome.