Lymphotoxin-β-deficient mice show defective antiviral immunity
Lymphotoxin-β-deficient mice show defective antiviral immunity
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DOI：
10.1006/viro.1999.9811
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发表时间：
1999-07-20
期刊：
影响因子：
3.7
通讯作者：
Oldstone, MBA
中科院分区：
文献类型：
--
作者：
Berger, DP;Naniche, D;Oldstone, MBA
淋巴毒素β(LTβ)是肿瘤坏死因子家族的成员之一，在淋巴器官发生中发挥重要作用。为了确定LTβ是否参与细胞免疫，我们研究了LTβ缺陷(LTβ-/-)小鼠对淋巴细胞性脉络膜脑膜炎病毒(LCMV)的抗病毒免疫应答。细胞毒性T淋巴细胞(CTL)对LCMV的反应严重减弱，导致病毒在脑和肾脏持续存在。然而，LTβ缺陷的T淋巴细胞和树突状细胞的主要功能是完整的。用LTβ/-骨髓重建受照射的LTβ/+小鼠，可导致脾结构紊乱，并伴有LCMV特异性CTL反应的损害。这些数据表明，LTβ的缺失并不影响T淋巴细胞或树突状细胞的内在功能，但脾的结构完整性与抗病毒免疫的产生密切相关。(C)1999年学术出版社。
Lymphotoxin beta (LT beta), a member of the tumor necrosis factor family, plays an important role in lymphoid organogenesis. In order to determine whether LT beta is involved in cellular immunity, we investigated the antiviral immune response of LT beta-deficient (LT beta -/-) mice to lymphocytic choriomeningitis virus (LCMV). Cytotoxic T lymphocyte (CTL) responses to LCMV were severely diminished, leading to viral persistence in brain and kidney. However, major functions of LT beta-deficient T lymphocytes and dendritic cells were intact. Reconstitution of irradiated LT beta +/+ mice with LT beta -/- bone marrow induced a disorganized splenic structure, accompanied by impairment of the LCMV-specific CTL response. These data indicate that the absence of LT beta does not affect the intrinsic function of T lymphocytes or of dendritic cells but that the structural integrity of the spleen is strongly associated with generation of antiviral immunity. (C) 1999 Academic Press.