| First Author | Koh YI | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 7 | Pages | 4560-4569 |
| PubMed ID | 18802058 | Mgi Jnum | J:141297 |
| Mgi Id | MGI:3818093 | Doi | 10.4049/jimmunol.181.7.4560 |
| Citation | Koh YI, et al. (2008) Activation of nonclassical CD1d-restricted NK T cells induces airway hyperreactivity in beta2-microglobulin-deficient mice. J Immunol 181(7):4560-9 |
| abstractText | Allergic asthma is characterized by Th2-driven eosinophilic airway inflammation and by a central feature called airway hyperreactivity (AHR), development of which requires the presence of classical type I invariant NK T (iNKT) cells. Allergen-induced AHR, however, develops in beta(2)-microglobulin (beta(2)m)(-/-) mice, which lack classical iNKT cells, suggesting that in some situations iNKT cells may be dispensable for the development of AHR. In contrast, our studies now suggest that a CD1d-restricted, NK1.1(+) noninvariant TCR NKT cell population is present in beta(2)m(-/-) mice and is responsible for the development of AHR but not for Th2 responses. Furthermore, treatment of beta(2)m(-/-) mice with anti-CD1d mAb or anti-NK1.1 mAb unexpectedly abolished allergen-induced AHR. The CD1-restricted NKT cells in these mice, which failed to respond to alpha-galactosylceramide and which therefore were not classical type I iNKT cells, appear to represent an NKT cell subset restricted by a beta(2)m-independent form of CD1d. These results indicate that, although classical type I iNKT cells are normally required for the development of AHR, under different circumstances other NKT cell subsets, including nonclassical NKT cells, may substitute for classical iNKT cells and induce AHR. |
