Modification of the Sendai virus-specific antibody and CD8+ T-cell responses in mice homozygous for disruption of the interleukin-4 gene.
Modification of the Sendai virus-specific antibody and CD8+ T-cell responses in mice homozygous for disruption of the interleukin-4 gene.
复制标题
仙台病毒特异性抗体和纯合小鼠 CD8 T 细胞反应的修饰,以破坏白细胞介素 4 基因。
DOI:
10.1128/jvi.71.3.2518-2521.1997
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发表时间:
1997
期刊:
影响因子:
--
通讯作者:
Doherty,PC
中科院分区:
文献类型:
--
作者:
Mo,XY;Sangster,MY;Tripp,RA;Doherty,PC
Homozygous disruption (-/-) of the interleukin-4 (IL-4) gene did not obviously modify the severity of Sendai virus infection in the highly susceptible 129/J mouse strain. The virus was cleared from the respiratory tract, and potent cytotoxic T lymphocyte (CTL) effectors were present in the cell population recovered by bronchoalveolar lavage. However, the prevalence of virus-specific CTL precursors (p) was consistently diminished in the spleen and regional lymph nodes of the IL-4 -/- mice at day 7 after infection. Also, virus-specific serum immunoglobulin G1 (IgG1) levels were greatly reduced and few IgG1-producing cells were detected in the lymphoid tissue. The effect on IgG1 class switching was to be expected, but the decrease in CTLp numbers has not been observed previously for a virus-specific immune response.