The aberrant expression of stimulatory and inhibitory killer immunoglobulin-like receptors in NK- and NKT-cells contributes to lupus

Clin Lab. 2014;60(5):717-27. doi: 10.7754/clin.lab.2013.130435.

Abstract

Background: Killer cell immunoglobulin-like receptors (KIR) contribute to the pathogenesis of multiple auto-immune diseases via the modulation of NK-, NKT- and T-cells. Thus, we want to know whether the expression pattern of KIR is associated with systemic lupus erythematosus (SLE) susceptibility.

Methods: Here, real-time quantitative PCR and fluorescence-activated cell sorting (FACS) were used to measure the stimulatory KIR (sKIR) and inhibitory KIR (iKIR) mRAN and protein levels on NK-, NKT- and T-cells in both SLE patients and healthy controls.

Results: In SLE patients, CD158a/h (KIR2DL1/S1) was highly expressed while CD158b/i/j (KIR2DL2/L3/S2, iKIR/iKIR/sKIR) was lowly expressed in NK- and NKT-cells in patients. The expression levels of KIR2DL1 and KIR2DL2 (iKIRs) were decreased while the expression levels of KIR2DS1 (sKIR) were increased in NK- and NKT-cells in the patients.

Conclusions: We found that SLE patients represent aberrant expression of stimulatory and inhibitory KIRs in NK- and NKT-cells. Consequently, these different expression levels of KIRs may contribute to the abnormal function of these cells, which lead to the risk of SLE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Case-Control Studies
  • Female
  • Genetic Predisposition to Disease
  • Humans
  • Killer Cells, Natural / metabolism*
  • Killer Cells, Natural / pathology
  • Lupus Erythematosus, Systemic / genetics
  • Lupus Erythematosus, Systemic / immunology*
  • Lupus Erythematosus, Systemic / pathology
  • Male
  • Natural Killer T-Cells / metabolism*
  • Natural Killer T-Cells / pathology
  • Receptors, KIR / biosynthesis
  • Receptors, KIR / genetics
  • Receptors, KIR / metabolism*
  • Receptors, KIR2DL2 / biosynthesis
  • Receptors, KIR2DL2 / genetics
  • Receptors, KIR2DL2 / metabolism*
  • Risk Assessment
  • Young Adult

Substances

  • KIR2DL2 protein, human
  • KIR2DS1 protein, human
  • Receptors, KIR
  • Receptors, KIR2DL2