Lymphotoxin-alpha-deficient mice can clear a productive infection with murine gammaherpesvirus 68 but fail to develop splenomegaly or lymphocytosis.
Lymphotoxin-alpha-deficient mice can clear a productive infection with murine gammaherpesvirus 68 but fail to develop splenomegaly or lymphocytosis.
复制标题
淋巴毒素-α 缺陷小鼠可以清除鼠伽马疱疹病毒 68 的有效感染，但不会出现脾肿大或淋巴细胞增多。
DOI：
10.1128/jvi.74.6.2786-2792.2000
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发表时间：
2000
影响因子：
5.4
通讯作者：
Sarawar,SR
中科院分区：
文献类型：
--
作者：
Lee,BJ;Santee,S;VonGesjen,S;Ware,CF;Sarawar,SR
Respiratory challenge with murine gammaherpesvirus 68 (MHV-68) leads to an acute productive infection of the lung and a persistent latent infection in B lymphocytes, epithelia, and macrophages. The virus also induces splenomegaly and an increase in the number of activated CD8 T cells in the circulation. Lymphotoxin- α-deficient (LTα−/−) mice have no lymph nodes and have disrupted splenic architecture. Surprisingly, in spite of the severe defect in secondary lymphoid tissue, LTα−/−mice could clear a productive MHV-68 infection, although with delayed kinetics compared to wild-type mice, and could control latent infection. Cytotoxic T-cell activity was comparable in the lungs and spleens of LTα−/−and wild-type mice. However, splenic gamma interferon responses were substantially reduced in LTα−/−mice. Furthermore, LTα−/−mice failed to develop splenomegaly or lymphocytosis. Although germinal centers were absent, LTα−/−mice were able to class switch and showed significant virus-specific antibody titers. This work demonstrates that organized secondary lymphoid tissue is not an absolute requirement for the generation of immune responses to viral infections.
