共 44 条
S1P1 receptor signaling overrides retention mediated by Gαi-coupled receptors to promote T cell egress
被引:345
作者:

Pham, Trung H. M.
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h-index: 0
机构:
Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA

Okada, Takaharu
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h-index: 0
机构:
Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA

Matioubian, Mehrdad
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h-index: 0
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Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA

Lo, Charles G.
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h-index: 0
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Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA

Cyster, Jason G.
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h-index: 0
机构:
Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
机构:
[1] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
来源:
关键词:
D O I:
10.1016/j.immuni.2007.11.017
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
The mechanism by which sphingosine-1-phosphate receptor-1 (S1P(1)) acts to promote lymphocyte egress from lymphoid organs is not defined. Here, we showed that CCR7-deficient T cells left lymph nodes more rapidly than wild-type cells did, whereas CCR7-overexpressing cells were retained for longer. After treatment with FTY720, an agonist that causes down-modulation of lymphocyte S1P(1), CCR7-deficient T cells were less effectively retained than wild-type T cells. Moreover, treatment with pertussis toxin to inactivate signaling via G alpha(i)-protein-coupled receptors restored egress competence to S1P(1)-deficient lymphocytes. We also found that T cell accumulation in lymph node cortical sinusoids required intrinsic S1P(1) expression and was antagonized by CCR7. These findings suggest a model where S1P(1) acts in the lymphocyte to promote lymph node egress by overcoming retention signals mediated by CCR7 and additional G alpha(i)-coupled receptors. Furthermore, by simultaneously upregulating S1P(1) and downregulating CCR7, T cells that have divided multiple times switch to a state favoring egress over retention.
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页码:122 / 133
页数:12
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