http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Thangada, Shobha,Khanna, Kamal M.,Blaho, Victoria A.,Oo, Myat Lin,Im, Dong-Soon,Guo, Caiying,Lefrancois, Leo,Hla, Timothy The Rockefeller University Press 2010 The Journal of experimental medicine Vol.207 No.7
<P>The sphingosine 1-phosphate receptor 1 (S1P<SUB>1</SUB>) promotes lymphocyte egress from lymphoid organs. Previous work showed that agonist-induced internalization of this G protein–coupled receptor correlates with inhibition of lymphocyte egress and results in lymphopenia. However, it is unclear if S1P<SUB>1</SUB> internalization is necessary for this effect. We characterize a knockin mouse (<I>S1p1r<SUP>S5A/S5A</SUP></I>) in which the C-terminal serine-rich S1P<SUB>1</SUB> motif, which is important for S1P<SUB>1</SUB> internalization but dispensable for S1P<SUB>1</SUB> signaling, is mutated. T cells expressing the mutant S1P<SUB>1</SUB> showed delayed S1P<SUB>1</SUB> internalization and defective desensitization after agonist stimulation. Mutant mice exhibited significantly delayed lymphopenia after S1P<SUB>1</SUB> agonist administration or disruption of the vascular S1P gradient. Adoptive transfer experiments demonstrated that mutant S1P<SUB>1</SUB> expression in lymphocytes, rather than endothelial cells, facilitated this delay in lymphopenia. Thus, cell-surface residency of S1P<SUB>1</SUB> on T cells is a primary determinant of lymphocyte egress kinetics in vivo.</P>