| First Author | Segawa S | Year | 2011 |
| Journal | Am J Respir Cell Mol Biol | Volume | 45 |
| Issue | 3 | Pages | 659-66 |
| PubMed ID | 21257923 | Mgi Jnum | J:190220 |
| Mgi Id | MGI:5448388 | Doi | 10.1165/rcmb.2010-0298OC |
| Citation | Segawa S, et al. (2011) Involvement of NK 1.1-positive gammadeltaT cells in interleukin-18 plus interleukin-2-induced interstitial lung disease. Am J Respir Cell Mol Biol 45(3):659-66 |
| abstractText | Interstitial lung disease (ILD) is induced by various factors in humans. However, the exact mechanism of ILD remains elusive. This study sought to determine the role of natural killer (NK) 1.1(+) gammadeltaT cells in ILD. The injection of IL-18 plus IL-2 (IL-18/IL-2) into C57BL6 (B6) mice induced acute ILD that resembled early-stage human ILD. An accumulation of NK1.1(+) gammadeltaT cells similar to NK cells was evident in the lungs. The T Cell Receptor (TCR) Vgamma and Vdelta repertoires of NK1.1(+) gammadeltaT cells indicated polyclonal expansion. The expression of IL-2 receptor beta (Rbeta) and IL-18Rbeta in NK1.1(+) gammadeltaT cells was higher than in NK1.1(-) gammadeltaT cells. IL-18/IL-2 stimulated the proliferation of NK1.1(+) gammadeltaT cells, but not NK1.1(-) gammadeltaT cells. The IL-18/IL-2-stimulated NK1.1(+) gammadeltaT cells produced higher concentrations of IFN-gamma than did NK1.1(-) gammadeltaT cells. Moreover, NK1.1(+) gammadeltaT and NK1.1(-) gammadeltaT cells constituted completely different cell populations. The IL-18/IL-2-induced ILD was milder in TCRdelta(-/-) and IFN-gamma(-/-) mice, compared with B6 mice. Furthermore, cell-transfer experiments demonstrated that NK1.1(+) gammadeltaT cells could induce the expansion of NK cells and IFN-gamma mRNA in the lung by IL-18/IL-2. Our results suggest that NK1.1(+) gammadeltaT cells function as inflammatory mediators in the early phase of IL-18/IL-2-induced ILD. |
