Microarray Analysis of Host Immune Responses to Marek's Disease Virus Infection in Vaccinated Chickens
Microarray Analysis of Host Immune Responses to Marek's Disease Virus Infection in Vaccinated Chickens
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DOI:
10.1292/jvms.71.603
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发表时间:
2009-05-01
影响因子:
1.2
通讯作者:
Ohashi, Kazuhiko
中科院分区:
文献类型:
--
作者:
Kano, Rika;Konnai, Satoru;Ohashi, Kazuhiko
Marek's disease (MD) is a commercially important disease of chickens caused by MD virus (MDV). Although avirulent MDV strains have been used for vaccination to prevent MD outbreaks, the protective mechanism of the vaccine has not been elucidated. In this Study, a comprehensive transcriptional analysis using microarray wits conducted in MDV-infected chickens with and without vaccination at 7 and 21 days post-infection (dpi). The data Suggested that the expression of T cell receptor (TCR) 1-related genes was up-regulated in vaccinated-challenged compared to unvaccinated-challenged chickens during the latent phase of infection. Consistently, this induction was confirmed by quantitative PCR. Flow cytometric analysis revealed that most of TCR1(+) cells expressed CD8 alpha chain brightly. The number of this subpopulation was significantly and specifically increased in vaccinated-challenged chickens at 21 dpi compared to univaccinated-challenged chickens, though it was not the major Population in spleen of chickens. The number of CD8 alpha(high) TCR2(+) cells, the major subpopulation of chicken CD8 alpha(high) cells, was increased in vaccinated chickens with or without challenge compared to univaccinated control chickens. These data suggested that both CD8 alpha(high) TCR1(+) and CD8 alpha(high) TCR2(+) cells could be induced by the vaccination. It is also possible that CD8 alpha(high) TCR1(+) cells might be primed by the vaccination and specifically induced by the challenge with virulent strain of MDV during the latent phase of infection. Thus, CD8 alpha(high) TCR1(+) cell Population is probably one of the key factors involved in the protective mechanism induced by a vaccine strain, CV1988.