| First Author | Hao J | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 2 | Pages | e57495 |
| PubMed ID | 23469004 | Mgi Jnum | J:197263 |
| Mgi Id | MGI:5491984 | Doi | 10.1371/journal.pone.0057495 |
| Citation | Hao J, et al. (2013) Nicotinic receptor beta2 determines NK cell-dependent metastasis in a murine model of metastatic lung cancer. PLoS One 8(2):e57495 |
| abstractText | Cigarette smoke exposure markedly compromises the ability of the immune system to protect against invading pathogens and tumorigenesis. Nicotine is a psychoactive component of tobacco products that acts as does the natural neurotransmitter, acetylcholine, on nicotinic receptors (nAChRs). Here we demonstrate that natural killer (NK) cells strongly express nAChR beta2. Nicotine exposure impairs the ability of NK cells to kill target cells and release cytokines, a process that is largely abrogated by nAChR beta2 deficiency. Further, nicotinic suppression of NF-kappaB-induced transcriptional activity in NK cells is dependent on nAChR beta2. This nAChR subtype also plays a large role in the NK cell-mediated control of melanoma lung metastasis, in a murine lung metastasis model exposed to nicotine. Our findings suggest nAChR beta2 as a prominent pathway for nicotine induced impairment of NK cell functions which contributes to the occurrence of smoking-related pathologies. |
