Innate lymphoid cell disturbance with increase in ILC1 in systemic lupus erythematosus
The innate lymphoid cell (ILC) is a group of effector cells with diverse important cellular functions in both health and disease states. In comparison with healthy controls, there were increases in circulating ILC in SLE patients. The proportion of ILC1 significantly increased with significant decre...
Saved in:
Published in | Clinical immunology (Orlando, Fla.) Vol. 202; pp. 49 - 58 |
---|---|
Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.05.2019
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | The innate lymphoid cell (ILC) is a group of effector cells with diverse important cellular functions in both health and disease states. In comparison with healthy controls, there were increases in circulating ILC in SLE patients. The proportion of ILC1 significantly increased with significant decreases of ILC2 in SLE patients and ILC3 in SLE patients with moderate to severe activity. IL-12, IL-18, IL-25, IL-33, IL-23, IL-1β and IFN-γ were significantly increased in SLE patients. Moreover, IL-12, IL-18 and IL-1β but not IFN-γ correlated significantly with SLEDAI. Successful treatments rapidly reduced them and with certain normalization of the ILC subsets. In addition to increases in ILC1 numbers, ~ 80% of the ILC1 in SLE patients were positive for synthesis of IFN-γ. Plasma from SLE patients were shown to be potent in inducing ILC1. Thus, increased circulating ILC1 might contribute to the pathogenesis of SLE through mounting type 1 immune response.
•Frequencies of ILCs were increased in SLE and majority of increased ILC subsets were ILC1.•Levels of IL-12 and IL-18 were increased and positively correlated with ILC1 in SLE.•Circulating ILC1 might contribute to the pathogenesis of SLE through mounting type 1 immune response. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contribute equally to this work. |
ISSN: | 1521-6616 1521-7035 1521-7035 |
DOI: | 10.1016/j.clim.2019.03.008 |