Journal
MEDIATORS OF INFLAMMATION
Volume 2016, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2016/9675861
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Funding
- National Science Council of Republic of China [MOST103-2314-B-182A-023-MY3]
- Division of Asthma, Allergy, and Rheumatology, Department of Pediatrics, Chang Gung Children's Hospital [CMRPG4A0052, CMRPG3D1933]
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Adhesion molecules may play an important role in systemic lupus erythematosus (SLE) pathogenesis. We investigated the effect of interleukin- (IL-) 15 on CD11b, CD54, and CD62L expression on natural killer (NK) cells, T cells, and CD56(+) CD3(+) NKT-like cells from SLE subjects and healthy controls. SLE patients had decreased circulating NK cells and NKT-like cells compared to controls. NK cells from SLE patients showed higher CD11b and CD62L expression compared to controls. IL-15 enhanced CD11b and CD54 but downregulated CD62L expression on NK cells from SLE patients. Similar observations were found for T cells and NKT-like cells. NK cells from SLE patients expressed higher CD56 than controls; both could be further enhanced by IL-15. IL-15 also enhanced CD56 expression of NKT-like cells from SLE patients. A greater degree of IL-15 induced downregulation of CD62L on NKT-like cells noted in SLE patients compared to controls. The percentage of CD11b expressing NK cells and the % inhibition of CD62L expressiononNKT-like cells by IL-15 correlatedwithserumanti-dsDNA levels in SLEpatients, respectively. Taken together, we demonstrated the dysfunctionalNK and NKT-like cells in SLE patients with regard to CD11b and CD62L expression and their response to IL-15.
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