Accelerated progression of a murine retrovirus-induced immunodeficiency syndrome in fas mutant C57BL/6 lpr/lpr mice

Kenji Hiromatsu, Jun Usami, Yoshiyasu Aoki, Masahiko Makino, Yasunobu Yoshikai

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    5 Citations (Scopus)

    Abstract

    We reported previously that CD4+ T cells and B cells in mice with retrovirus-induced murine acquired immunodeficiency syndrome (MAIDS) caused by LP-BM5 murine leukemia virus (MuLV) mixtures increased the expression of Fas antigen (Fas) during progression of the disease. However, the contribution of the Fas/Fas ligand (Fas L) system to the pathogenesis of MAIDS remained unknown. Here, we examined the susceptibility of C57BL/6 (B6) lpr/lpr mice, which has been reported to be defective for the expression of Fas, to MAIDS. We found that the Thy1.2-CD4 T cells and Igκ dull B220+ cells, which are characteristic of MAIDS, increased after the inoculation of LP-BM5 MuLV in B6 lpr/lpr mice. B220+ TCR αβ T cells, unique to lupus prone mice, also increased in the B6 lpr/lpr mice after infection. CD4+ B220+ TCR αβ T cells increased profoundly among the B220+ TCR αβ T cells from LP-BM5 MuLV-infected B6 lpr/lpr mice, while the B220+ TCR αβ T cells observed in non-infected B6 lpr/lpr mice were largely of the CD4- CD8- phenotype. A DNA PCR analysis of the LP-BM5 MnLV-infected B6 lpr/lpr mice revealed the genome integration of defective LP-BM5 virus, further confirming that MAIDS is inducible to B6 lpr/lpr mice. LP-BM5 MuLV-infected lpr/lpr mice died within 3 months, while MAIDS-infected B6 +/+ mice usually died within 5 to 6 months, and B6 lpr/lpr mice not infected with LP-BM5 MuLV lived more than 6 months. Taken together, these results suggest that MAIDS is inducible independently with functional Fas expression and the possibility of accelerated progression of murine AIDS and lpr-associated autoimmune disease in B6 lpr/lpr mice infected with LP-BM5 MuLV.

    Original languageEnglish
    Pages (from-to)221-227
    Number of pages7
    JournalMICROBIOLOGY and IMMUNOLOGY
    Volume41
    Issue number3
    DOIs
    Publication statusPublished - Jan 1 1997

    All Science Journal Classification (ASJC) codes

    • Microbiology
    • Immunology
    • Virology

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