Ohteki T, Maki C, Koyasu S, Mak T W, Ohashi P S
Department of Medical Biophysics, Ontario Cancer Institute, Toronto, Canada.
J Immunol. 1999 Apr 1;162(7):3753-6.
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.
利用缺乏淋巴细胞功能相关抗原-1（LFA-1）、淋巴细胞归巢受体CD44和细胞间黏附分子-1（ICAM-1）的小鼠，我们研究了这些黏附分子在NK1.1⁺TCRαβ⁺（NKT）细胞发育中的作用。尽管在CD44基因敲除小鼠和ICAM-1基因敲除小鼠中未观察到NKT细胞发育缺陷，但在LFA-1基因敲除小鼠中，肝脏NKT细胞显著减少。LFA-1基因敲除小鼠的其他淋巴器官中存在正常数量的NKT细胞。当将LFA-1基因敲除小鼠的脾细胞静脉注射到野生型小鼠体内时，受体肝脏中供体来源细胞中的NKT细胞频率正常。相反，当将LFA-1基因敲除小鼠的骨髓（BM）细胞静脉注射到经辐照的野生型小鼠体内时，肝脏NKT细胞的频率显著低于注射野生型BM细胞的小鼠。总体而言，这些数据表明LFA-1是肝脏NKT细胞发育所必需的，而不是成熟NKT细胞向肝脏迁移和/或随后在肝脏中定植所必需的。
