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  • Title: Characterization of mouse mammary tumour virus-induced migration of lymphoid cells into lymph nodes.
    Author: Matsuzawa A, Yasuda T, Sakamoto S, Nagase H, Nakano H, Yoshimoto T.
    Journal: Scand J Immunol; 2001 Jun; 53(6):553-62. PubMed ID: 11422903.
    Abstract:
    We previously found that Mtv-2+ lymph nodes (LN) implanted into Mtv-2- mice underwent marked hyperplasia owing to the influx of lymphocytes. LN grafts infected with exogenous mouse mammary tumour viruses (MMTV), MMTV(FM) transmitted by FM mice and MMTV-2 produced by Mtv-2, also swelled in MMTV-free recipients. Mtv-3 and Mtv-7 also displayed this capability. Mtv-2-induced LN hyperplasia was earlier in onset and greater in extent when major histocompatibility complex (MHC) class II I-E was expressed than unexpressed. Mtv-3-induced LN hyperplasia was suppressed completely by Mtv-3 from a different mouse strain and partially by Mtv-6 slightly different from Mtv-3 in superantigen (SAg) Vbeta specificity. LN hyperplasia occurred bidirectionally in LN transplantation between mice carrying Mtv-2 and Mtv-3, which are different SAg Vbeta specificity. LN hyperplasia induced by MMTV-2 carrying SAg responsive to Vbeta14 alone and MMTV(FM) carrying SAg responsive to Vbeta14 and Vbeta8.2 was completely but partially suppressed by MMTV(FM) and MMTV-2, respectively. CD4+ T cells were essential for MMTV-induced LN hyperplasia. LN in situ also underwent significant hyperplasia when infected with MMTV. Thus, MMTV SAg may entice circulating lymphocytes into lymphoid organs and contribute to more efficient dissemination MMTV in vivo. Secondary lymphoid tissue chemokine (SLC) may not be directly involved in this event.
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