CD27 natural killer cell subsets play different roles during the pre-onset stage of experimental autoimmune encephalomyelitis

Abstract

NK cells participate in the development of human multiple sclerosis (MS) and mouse experimental autoimmune encephalomyelitis (EAE), but the roles of different NK cell subsets in disease onset remain poorly understood. In this study, murine NK cells were divided into CD27(high) and CD27(low/-) subsets. The CD27(high) subset was decreased and the CD27(low/-) subset was increased in lymphoid organs during the pre-onset stage of EAE. Compared with the counterpart in naïve mice, the CD27(high) subset showed lower expression of Ly49D, Ly49H and NKG2D, and less production of IFN-γ, whereas the CD27(low/-) subset showed similar expression of the above mentioned surface receptors but higher cytotoxic activity in EAE mice. Compared with the CD27(high) subset, the CD27(low/-) subset exhibited increased promotion of DC maturation and no significant inhibition of T cells proliferation and Th17 cells differentiation in vitro Additionally, adoptive transfer of the CD27(low/-) subset, but not the CD27(high) subset, exacerbated the severity of EAE. Collectively, our data suggest the CD27 NK cell subsets play different roles in controlling EAE onset, which provide a new understanding for the regulation of NK cell subsets in early autoimmune disease.

The Important Role of Dendritic Cell (DC) in iNKT-Mediated Modulation of NK Cell Function in Chlamydia pneumoniae Lung Infection

“…More interestingly, the data provided in vivo evidence of NK subset switch in response to Cpn infection. Distinct function of NK subsets based on CD27 and CD11b expression has been reported [12, 37, 38]. We observed that Cpn infection increased the percentage of CD11b low CD27 high and CD11b high CD27 high NK subsets so consequently reducing the proportion of CD11b high CD27 low NK subset.…”

“…Among these subsets, the CD11b low CD27 high and CD11b high CD27 high subsets exhibit enhanced cytokine production and higher responsiveness, while CD11b high CD27 low NK subsets appear to be more tightly controlled due to their higher expression of inhibitory receptors [11]. The functional distinctions of NK subsets in immune responses have been discerned in several disease models [12, 13].…”

Peripheral and Central Neuroinflammatory Changes and Pain Behaviors in an Animal Model of Multiple Sclerosis

“…In parallel with another recent study ( 17 ), we found increased numbers of infiltrating CD4+ cells in the DRG in clinical EAE, where it has been previously reported that rats with EAE have elevated expression of fractalkine (CX3CL1) and its receptor (CX3CR1) ( 59 ), and increased levels of TNF-α ( 60 , 61 ), and IL-1β ( 62 ). Innate immune cells such as NK cells, neutrophils, and mast cells are also known to be involved in the pathogenesis of EAE ( 63 – 65 ); however, their role in pain associated with EAE and MS is unclear. Mast cells in particular have been implicated in the production of neuropathic pain in models of peripheral nerve injury ( 66 ) and chemotherapy-induced peripheral neuropathy ( 67 ).…”

The Increased Ratio of Blood CD56bright NK to CD56dim NK Is a Distinguishing Feature of Primary Sjögren’s Syndrome

“…NK cells are characterized conventionally by the expression of the CD56 surface marker [15,16]. Based on the expression of CD56, human NK cells are divided into CD56 bright and CD56 dim subsets [17]. It is commonly recognized that CD56 bright NK cells account for about 10% of human peripheral blood NK cells mainly producing various cytokines and chemokines, whereas CD56 dim NK cells account for about 90% of human peripheral blood NK cells with higher cytotoxic [9,18,19].…”