ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 1063

Dysfunction of Natural Killer and Natural Killer T Cells in Patients with Adult Onset Still’s Disease

Young-Nan Cho1, Sung-Ji Lee1, Tae-Jong Kim2, Hye-Mi Jin1, Dong-Jin Park2, Seung-Jung Kee3 and Yong-Wook Park1, 1Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, South Korea, 2Rheumatology, Chonnam National University Medical School, Gwangju, South Korea, 3Laboratory Medicine, Chonnam National University Medical School and Hospital, Gwangju, South Korea

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: ,

Session Information

Title: Innate Immunity and Rheumatic Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose: Adult onset Still’s disease (AOSD) is an uncommon systemic inflammatory disorder of unknown etiology. Natural killer (NK) cell dysfunction is frequently observed in some human autoimmune disease, such as systemic lupus erythematosus and rheumatoid arthritis. However, NK cell function has not previously been investigated in AOSD. Furthermore, the relation between NK and NKT cells has not been determined. Purpose of this study is to examine the levels and functions of NK and NKT cells, to investigate relationships between NK and NKT cells, and to determine the clinical relevance of NKT cell levels in patients with AOSD.

Methods: Patients with active untreated AOSD (n = 25) and age- and sex-matched healthy controls (n = 25) were enrolled in the study. NK and NKT cell levels were measured by flow cytometry. Peripheral blood mononuclear cells were cultured in vitro with α-galactosylceramide (α-GalCer). NK cytotoxicities against K562 cells and proliferation indices of NKT cells were estimated by flow cytometry.

Results: Percentages and absolute numbers of NKT cells were significantly lower in the peripheral blood of patients than in healthy controls. Proliferative responses of NKT cells to α-GalCer were also lower in patients, and this was found to be due to proinflammatory cytokines and NKT cell apoptosis. In addition, NK cytotoxicities were found to be significantly lower in patients than in healthy controls, but NK cell levels were comparable in the two groups. Notably, this NKT cell deficiency was found to be correlated with NK cell dysfunction and to reflect an active disease status. Furthermore, α-GalCer-mediated NK cytotoxicity, showing the interaction between NK and NKT cells, was significantly lower in patients than in healthy controls.

Conclusion:

Our findings show that NKT cells are numerically and functionally deficient in AOSD. In addition, we report a novel observation that NK cell dysfunction is related to NKT cell deficiency. These findings provide important information concerning the pathogenesis of AOSD.

Disclosure:

Y. N. Cho,
None;

S. J. Lee,
None;

T. J. Kim,
None;

H. M. Jin,
None;

D. J. Park,
None;

S. J. Kee,
None;

Y. W. Park,
None.

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