title: Sulfatide-activated type II NKT cells prevent allergic airway inflammation by inhibiting type I NKT cell function in a mouse model of asthma.
abstract: Asthma is a common chronic inflammatory disease involving many different cell types. Recently, type I natural killer T (NKT) cells have been demonstrated to play a crucial role in the development of asthma. However, the roles of type II NKT cells in asthma have not been investigated before. Interestingly, type I and type II NKT cells have been shown to have opposing roles in antitumor immunity, antiparasite immunity, and autoimmunity. We hypothesized that sulfatide-activated type II NKT cells could prevent allergic airway inflammation by inhibiting type I NKT cell function in asthma. Strikingly, in our mouse model, activation of type II NKT cells by sulfatide administration and adoptive transfer of sulfatide-activated type II NKT cells result in reduced-inflammation cell infiltration in the lung and bronchoalveolar lavage fluid, decreased levels of IL-4 and IL-5 in the BALF; and decreased serum levels of ovalbumin-specific IgE and IgG1. Furthermore, it is found that the activation of sulfatide-reactive type II NKT cells leads to the functional inactivation of type I NKT cells, including the proliferation and cytokine secretion. Our data reveal that type II NKT cells activated by glycolipids, such as sulfatide, may serve as a novel approach to treat allergic diseases and other disorders characterized by inappropriate type I NKT cell activation.
authors.affiliation: Department of Respiratory Medicine, Zhongnan Hospital of Wuhan University, China.
authors.forename: Guqin
authors.initials: G
authors.lastname: Zhang
authors.forename: Hanxiang
authors.initials: H
authors.lastname: Nie
authors.forename: Jiong
authors.initials: J
authors.lastname: Yang
authors.forename: Xuhong
authors.initials: X
authors.lastname: Ding
authors.forename: Yi
authors.initials: Y
authors.lastname: Huang
authors.forename: Hongying
authors.initials: H
authors.lastname: Yu
authors.forename: Ruyou
authors.initials: R
authors.lastname: Li
authors.forename: Zhuqing
authors.initials: Z
authors.lastname: Yuan
authors.forename: Suping
authors.initials: S
authors.lastname: Hu
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000517:prevention & control*; D001992:Bronchoalveolar Lavage Fluid; D005260:Female; D020397:Goblet Cells / Q000187:drug effects / Q000473:pathology; D006965:Hyperplasia / Q000517:prevention & control; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D055611:Natural Killer T-Cells / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology / Q000637:transplantation; D010047:Ovalbumin; D020545:Respiratory Mucosa / Q000187:drug effects / Q000473:pathology; D013433:Sulfoglycosphingolipids / Q000494:pharmacology*
chemical_list: D007074:Immunoglobulin G; D015848:Interleukin-5; D013433:Sulfoglycosphingolipids; D015847:Interleukin-4; D007073:Immunoglobulin E; D010047:Ovalbumin