These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Functional and phenotypic change of T cells in murine acquired immune deficiency. Author: Kanagawa O, Gayama S, Vaupel B. Journal: J Immunol; 1994 May 01; 152(9):4671-9. PubMed ID: 8157980. Abstract: Infection of susceptible C57BL/6 mice with defective LP-BM5 murine leukemia virus causes disease termed murine acquired immune deficiency syndrome (MAIDS). The disease is characterized by lymphoadenopathy, hyperimmunoglobulinemia, and immune deficiency in both T and B cell functions. The development of disease requires the presence of mature T cells, especially CD4 T cells, and B cells. It has previously been shown that a B cell tumor line derived from MAIDS mouse stimulated a large fraction of unprimed T cells based on TCR V beta chain expression. This stimulatory activity was assumed to be mediated by a superantigen encoded by MAIDS virus. The stimulation of T cells by viral superantigen was thought to play a role in the development of the disease. To examine the role of T cell reactivity to MAIDS superantigen, we used TCR transgenic mice. There are two distinct T cell populations which can be distinguished based on their TCR expression and function in the TCR transgenic mice, one bearing the transgene derived alpha- and beta-chain TCR that is nonreactive to MAIDS superantigen and the other bearing an endogenous alpha- but transgene-derived beta-chain TCR that is reactive to superantigen. Unlike T cells found in noninfected TCR transgenic mice, anergic T cells expanding in virally infected TCR transgenic mice are homogeneous for the TCR phenotype, indicating the presence of a selection of T cells based on their TCR expression. T cell hybridomas established by fusing T cells from virus-infected transgenic mice to thymoma cell line are also anergic. We found mRNA of defective LP-BM5 virus in a majority of T cell hybridomas from virus-infected mice but not from noninfected mice. By using in vitro infection of T cell clones with recombinant virus containing LP-BM5 MAIDS virus gag gene, we have demonstrated that virus infection directly abrogated the Ag-specific reactivity of T cells. The establishment of anergic T cell hybridomas and the in vitro infection of T cells with recombinant viruses would be a useful tool in the analysis of biochemical and molecular mechanisms of T cell dysfunction in MAIDS.[Abstract] [Full Text] [Related] [New Search]