Differential expression of natural killer activating and inhibitory receptors in patients with newly diagnosed systemic lupus erythematosus.

Abstract:

AIM:Systemic lupus erythematosus (SLE) presents as the abnormal activation and over-proliferation of immune competent cells. Few studies have characterized the role of natural killer (NK) and NK T (NKT) cells in the pathogenesis of SLE, and therefore a consensus has not been reached as yet. METHOD:Thirty-two patients with new-onset SLE and 15 healthy controls were recruited. Activated and inhibitory NK and NKT cells in peripheral blood were quantified by flow cytometry. The proportions of spontaneous and stimulated interferon (IFN)-γ(+) NK and NKT cells and CD107a(+) NK cells was examined. Finally, the potential relationship between the cell subsets and clinical indexes was analyzed. RESULTS:The proportions of NK and NKT cells (P = 0.002 and 0.004, respectively) as well as the proportions of NKG2C(+) NK cells, inhibitory NK and NKT cell subsets (P = 0.016, P = 0.019, P = 0.049, and P = 0.028, respectively) in SLE patients were significantly lower than those in controls. In contrast, the proportions of activated NK cells and NKT cell subsets were significantly higher (P = 0.036, P = 0.034, P = 0.005, and P = 0.007, respectively). Moreover, the proportions of stimulated IFN-γ(+) NKT cells were significantly higher than in the controls, and the proportions of stimulated CD107a(+) NKT cells in SLE patients were significantly lower than in the controls (P = 0.032 and P = 0.02, respectively). CONCLUSION:Lower proportions of NK and NKT cells, higher proportions of activated NK cells and activated NKT cells, lower proportions of inhibitory NK and NKT cells, higher NKT cell activity, and lower NKT cell degranulation may induce the autoimmune reaction involved in the pathogenesis of SLE.

journal_name

Int J Rheum Dis

authors

Ye Z,Ma N,Zhao L,Jiang ZY,Jiang YF

doi

10.1111/1756-185X.12289

subject

Has Abstract

pub_date

2016-06-01 00:00:00

pages

613-21

issue

6

eissn

1756-1841

issn

1756-185X

journal_volume

19

pub_type

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