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Low levels of soluble CD1d protein alters NKT cell function in patients with rheumatoid arthritis

Seiji Segawa1, Daisuke Goto, Yohei Yoshiga

  • 1Division of Clinical Immunology, Doctoral Program in Clinical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Japan.

International Journal of Molecular Medicine
|September 3, 2009
PubMed

Insights

Soluble CD1d (sCD1d) proteins are crucial for natural killer T (NKT) cell activation. Rheumatoid arthritis patients exhibit lower plasma sCD1d levels, potentially contributing to reduced NKT cell numbers and function.

Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • CD1d molecules present glycolipid antigens to natural killer T (NKT) cells.
  • Eight human CD1d splice variants exist, including a soluble form (sCD1d).

Purpose of the Study:

  • To investigate the role of soluble CD1d (sCD1d) in rheumatoid arthritis (RA).
  • To quantify plasma sCD1d levels and their correlation with NKT cells in RA patients.

Main Methods:

  • Generation of recombinant sCD1d proteins.
  • Quantification of plasma sCD1d using a newly established ELISA.
  • Analysis of NKT cell populations (TCR V alpha 24+ V beta 11+CD3+) in peripheral blood mononuclear cells.
  • Assay of sCD1d-induced cytokine production (IFN-gamma, IL-4, IL-10) from NKT cells.

Main Results:

  • Plasma sCD1d protein levels were significantly decreased in RA patients compared to healthy donors.
  • Plasma sCD1d levels correlated with the number of peripheral NKT cells.
  • sCD1d induced IFN-gamma production from NKT cells, but not IL-4 or IL-10.

Conclusions:

  • Low plasma sCD1d levels in RA patients may lead to reduced NKT cell numbers and activation.
  • sCD1d stimulates NKT cells, suggesting a role in RA pathogenesis.
  • Decreased sCD1d levels in RA could be a pathogenic mechanism linked to NKT cell reduction.

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