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

21Citations
Citations of this article
9Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

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. © The Japanese Society for Immunology. 2005. All rights reserved.

Cite

CITATION STYLE

APA

Kawabata, H., Niwa, A., Tsuji-Kawahara, S., Uenishi, H., Iwanami, N., Matsukuma, H., … Miyazawa, M. (2006). Peptide-induced immune protection of CD8+ T cell-deficient mice against Friend retrovirus-induced disease. International Immunology, 18(1), 183–198. https://doi.org/10.1093/intimm/dxh361

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free