SOCS1 deficiency causes a lymphocyte-dependent perinatal lethality
SOCS1 deficiency causes a lymphocyte-dependent perinatal lethality
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DOI：
10.1016/s0092-8674(00)80048-3
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发表时间：
1999-09-03
期刊：
影响因子：
64.5
通讯作者：
Ihle, JN
中科院分区：
文献类型：
--
作者：
Marine, JC;Topham, DJ;Ihle, JN
SOCS1.是一种含SH 2的蛋白，主要以细胞因子和T细胞受体非依赖性方式在胸腺细胞中表达。SOCS 1缺失导致围产期死亡，死亡时间为2-3周。在此期间，胸腺的变化包括细胞结构的丧失和从主要的CD 4（+）CD 8（+）转变为单个阳性细胞。外周T细胞表达活化抗原并在不存在抗CD 3的情况下增殖为IL-2。此外，IFN γ存在于血清中。用SOCS 1缺陷型干细胞重建JAK 3缺陷型小鼠的淋巴系，重现了致死性和T细胞改变。引入RAG 2或IFN γ缺陷消除了致死性。结果表明，淋巴细胞是至关重要的SOCS 1相关的围产期致死性和牵连SOCS 1淋巴细胞分化或调节。
SOCS1. is an SH2-containing protein that is primarily expressed in thymocytes in a cytokine- and T cell receptor-independent manner. SOCS1 deletion causes perinatal lethality with death by 2-3 weeks. During this period thymic changes include a loss of cellularity and a switch from predominantly CD4(+)CD8(+) to single positive cells. Peripheral T cells express activation antigens and proliferate to IL-2 in the absence of anti-CD3. In addition, IFN gamma is present in the serum. Reconstitution of the lymphoid lineage of JAK3-deficient mice with SOCS1-deficient stem cells recapitulates the lethality and T cell alterations. Introducing a RAG2 or IFN gamma deficiency eliminates lethality. The results demonstrate that lymphocytes are critical to SOCS1-associated perinatal lethality and implicate SOCS1 in lymphocyte differentiation or regulation.