title: Natural killer cells from patients with chronic rhinosinusitis have impaired effector functions.
abstract: Natural killer (NK) cells are multicompetent lymphocytes of the innate immune system that play a central role in host defense and immune regulation. Although increasing evidence suggests that innate immunity plays a key role in the pathogenesis of chronic rhinosinusitis (CRS), the role of NK cells in CRS has been poorly studied. This study aimed to characterize the peripheral blood NK cells from patients with CRS, and to compare the functions of these cells with those from non-CRS controls. The correlation between NK cell functional activity and prognosis was also assessed. Eighteen CRS patients and 19 healthy non-CRS controls were included. The patients with CRS were classified into two subgroups, namely a treatment-responsive group and recalcitrant group. NK cell degranulation was determined by measuring the cell surface expression of CD107a against 721.221 and K562 cells. Intracytoplasmic cytokine production was determined by flow cytometry. Compared to the controls, the NK cells of CRS group had an impaired ability to degranulate and to produce cytokines such as IFN-γ and TNF-α. The recalcitrant subgroup showed the most severe defects in NK cell effector functions. Moreover, the decreased NK cell functions in patients with CRS were associated with poor prognostic factors such as concomitant asthma and peripheral blood eosinophilia. NK cells, which were originally named for their ability to mediate spontaneous cytotoxicity towards diseased cells including infected cells, may play an important role in regulating the inflammatory process in CRS pathogenesis.
authors.affiliation: Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
authors.forename: Ji Heui
authors.initials: JH
authors.lastname: Kim
authors.forename: Gye Eun
authors.initials: GE
authors.lastname: Kim
authors.forename: Gye Song
authors.initials: GS
authors.lastname: Cho
authors.forename: Hyung-Joon
authors.initials: HJ
authors.lastname: Kwon
authors.forename: Chul Hyun
authors.initials: CH
authors.lastname: Joo
authors.forename: Hun Sik
authors.initials: HS
authors.lastname: Kim
authors.forename: Yong Ju
authors.initials: YJ
authors.lastname: Jang
mesh_terms: D000328:Adult; D001249:Asthma / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D016022:Case-Control Studies; D015550:Cell Degranulation / Q000276:immunology*; D002908:Chronic Disease; D004802:Eosinophilia / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D020014:K562 Cells; D007694:Killer Cells, Natural / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D012220:Rhinitis / Q000150:complications / Q000276:immunology* / Q000473:pathology; D012852:Sinusitis / Q000150:complications / Q000276:immunology* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000276:immunology
chemical_list: D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma