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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
Authors:Ohteki T  Maki C  Koyasu S  Mak T W  Ohashi P S
Affiliation:Department of Medical Biophysics, Ontario Cancer Institute, Toronto, Canada. tohteki@sun.microb.med.keio.ac.jp
Abstract: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 were 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.
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