| First Author | Ohteki T | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 7 | Pages | 3753-6 |
| PubMed ID | 10201888 | Mgi Jnum | J:53578 |
| Mgi Id | MGI:1332952 | Doi | 10.4049/jimmunol.162.7.3753 |
| Citation | Ohteki T, et al. (1999) Cutting edge: LFA-1 is required for liver NK1.1+TCR alpha beta+ cell development: evidence that liver NK1.1+TCR alpha beta+ cells originate from multiple pathways. J Immunol 162(7):3753-6 |
| abstractText | Using mice deficient for LFA-1, CD44, and ICAM-1, we examined the role of these adhesion molecules in NK1.1(+)TCR alpha beta(+) (NKT) cell development. Although no defect in NKT cell development was observed in CD44(-/- ) and ICAM-1(-/-) mice, a dramatic reduction of liver NKT cells was observed in LFA-1(-/-) mice. Normal numbers of NKT cells mere present in other lymphoid organs in LFA-1(-/ -) mice. When LFA-1(-/-) splenocytes were injected i.v. Into wild-type mice, the frequency of NKT cells among donor-derived cells in the recipient liver was normal. In contrast, when LFA-1(-/-) bone marrow (BM) cells were injected i.v. Into irradiated wild-type mice, the frequency of liver NKT cells was significantly lower than that of mice injected with wild-type BM cells. Collectively, these data indicate that LFA-1 is required for the development of liver NKT cells, rather than the migration to and/or subsequent establishment of mature NKT cells in the liver. |
