International Immunology Advance Access published online on December 13, 2005
International Immunology, doi:10.1093/intimm/dxh361
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1 Department of Immunology, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan
* To whom correspondence should be addressed. 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.
Received June 4, 2005
Accepted October 28, 2005
Article
Peptide-induced immune protection of CD8+ T cell-deficient mice against Friend retrovirus-induced disease
Hiroyuki Kawabata 1,
Atsuko Niwa 2,
Sachiyo Tsuji-Kawahara 1,
Hirohide Uenishi 3,
Norimasa Iwanami 4,
Hideaki Matsukuma 1,
Hiroyuki Abe 1,
Nobutada Tabata 5,
Haruo Matsumura 1,
and
Masaaki Miyazawa 1 *
2 Department of Immunology, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan; Present address: Department of Pharmacology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511, Japan
3 Genome Research Department, National Institute of Agrobiological Science, Tsukuba, Ibaraki 305-8602, Japan
4 Department of Immunology, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan; Present address: Division of Experimental Immunology, Institute for Genome Research, University of Tokushima, Tokushima 770-8503, Japan
5 Department of Immunology, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan; Present address: Department of Pediatrics, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511, Japan
Masaaki Miyazawa, E-mail: masaaki{at}med.kindai.ac.jp
Abstract 
2-microglobulin-deficient; CD4+ T; epitope; vaccine.
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