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Peptide-induced immune protection of CD8+ T cell-deficient mice against Friend retrovirus-induced disease

CD8+ CTLs and virus-neutralizing antibodies have been associated with spontaneous and vaccine-induced immune control of retroviral infections. We previously showed that a single immunization with an env gene-encoded CD4+ T cell epitope protected mice against fatal Friend retrovirus infection. Here,...

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Published in:International immunology 2006-01, Vol.18 (1), p.183-198
Main Authors: Kawabata, Hiroyuki, Niwa, Atsuko, Tsuji-Kawahara, Sachiyo, Uenishi, Hirohide, Iwanami, Norimasa, Matsukuma, Hideaki, Abe, Hiroyuki, Tabata, Nobutada, Matsumura, Haruo, Miyazawa, Masaaki
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Language:English
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Summary:CD8+ CTLs and virus-neutralizing antibodies have been associated with spontaneous and vaccine-induced immune control of retroviral infections. We previously showed that a single immunization with an env gene-encoded CD4+ T cell epitope protected mice against fatal Friend retrovirus infection. Here, we analyzed immune cell components required for the peptide-induced anti-retroviral protection. Mice lacking CD8+ T cells were nevertheless protected against Friend virus infection, while mice lacking B cells were not. Virus-producing cells both in the spleen and bone marrow decreased rapidly in their number and became undetectable by 4 weeks after infection in the majority of the peptide-immunized animals even in the absence of CD8+ T cells. In the vaccinated animals the production and class switching of virus-neutralizing and anti-leukemia cell antibodies were facilitated; however, virus-induced erythroid cell expansion was suppressed before neutralizing antibodies became detectable in the serum. Further, the numbers of virus-producing cells in the spleen and bone marrow in the early stage of the infection were smaller in the peptide-immunized than in unimmunized control mice in the absence of B cells. Thus, peptide immunization facilitates both early cellular and late humoral immune responses that lead to the effective control of the retrovirus-induced disease, but CD8+ T cells are not crucial for the elimination of virus-infected cells in the peptide-primed animals.
ISSN:0953-8178
1460-2377
DOI:10.1093/intimm/dxh361