Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1981 Feb;126(2):715-22.

Mechanisms in T cell leukemogenesis. II. T cell responses of preleukemic BALB/c mice to Moloney leukemia virus antigens

  • PMID: 6969759

Mechanisms in T cell leukemogenesis. II. T cell responses of preleukemic BALB/c mice to Moloney leukemia virus antigens

J C Lee et al. J Immunol. 1981 Feb.

Abstract

The T cell responses of Moloney leukemia virus (MoLV)-infected preleukemic BALB/c mice were examined. The major in vitro response detectable was T cell blastogenesis in response to the major viral envelope protein MoLV gp71 and an internal viral protein p12. The majority of the preleukemic mice had readily detectable responses to gp71, whereas the presence of a response to p12 was less consistent. With both antigens, T cell blastogenesis showed typical antigen response characteristics similar to those detected in other immune responses to C-type viruses. Proliferation was dependent on a Thy-1+, Lyt-1+, 2- population and was macrophage-independent. In contrast to most immune responses to C-type viruses, which are temporally restricted, T cell blastogenesis was detectable throughout the preleukemic period of 4 to 16 wk of age. During this period neither gp71-specific T cells nor PHA-responsive T cells were found to express viral antigens. The correlations between T cells responding to gp71 and leukemia were examined. Under conditions in which MoLV inoculation of BALB/c mice does not induce leukemia, no T cell responses were deectable. These results suggest a causal relationship between the presence of antigen-specific T cells and the ability of MoLV to induce leukemia. The results are discussed with reference to the possible role of chronic immune stimulation in virus-induced leukemogenesis.

PubMed Disclaimer

Similar articles

Cited by

Publication types

LinkOut - more resources