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Published on: August 21, 2017
CD14+CD16++ monocytes are increased in patients with NMO and are selectively suppressed by glucocorticoids therapy
Qiuming Zeng1, Xiaohua Dong1, Chunyun Ruan1
1Department of Neurology, Xiangya Hospital, Central South University, PR China.
Abstract:
The pathophysiologic significance of the CD16+ monocyte subset has been demonstrated by its expansion in various autoimmune disorders. To date, the characteristics and roles of monocyte subpopulations in patients with neuromyelitis optica (NMO) have been poorly defined. We measured the percentages of the monocyte subsets in the peripheral blood, the levels of IL-1β and TNF-α mRNA in monocyte subsets and the concentrations of IL-1β and TNF-α in plasma and CSF from NMO patients. Our results showed that nonclassical monocytes were up-regulated in NMO patients and significantly elevated IL-1β and TNF-α expression was detected in it. In addition the increased nonclassical monocytes could be selectively suppressed by GC in patients with NMO.
Insights
In neuromyelitis optica (NMO), nonclassical monocytes increase and show elevated IL-1β and TNF-α. Glucocorticoids (GC) effectively suppress these elevated monocytes in NMO patients.
Area of Science:
- Immunology
- Neuroimmunology
- Autoimmune Diseases
Background:
- CD16+ monocyte subset expansion is linked to autoimmune disorders.
- Monocyte subpopulations in neuromyelitis optica (NMO) remain poorly characterized.
- Understanding monocyte roles is crucial for NMO pathogenesis.
Purpose of the Study:
- To define monocyte subpopulation characteristics in NMO patients.
- To investigate IL-1β and TNF-α expression in NMO monocyte subsets.
- To assess the impact of glucocorticoids (GC) on NMO monocytes.
Main Methods:
- Quantified peripheral blood monocyte subsets in NMO patients.
- Measured IL-1β and TNF-α mRNA in monocyte subsets.
- Assessed IL-1β and TNF-α protein levels in plasma and cerebrospinal fluid (CSF).
Main Results:
- Nonclassical monocytes were significantly up-regulated in NMO patients.
- Elevated IL-1β and TNF-α expression was detected in nonclassical monocytes.
- Glucocorticoids selectively suppressed the increased nonclassical monocytes in NMO.
Conclusions:
- Nonclassical monocytes are implicated in NMO pathophysiology.
- Elevated IL-1β and TNF-α in nonclassical monocytes contribute to NMO.
- GC therapy demonstrates a targeted effect on pathogenic monocytes in NMO.
