Disease relevance of Mtv3

• Genes encoding endogenous superantigens causing Tcrb-V3+ T-cell deletion co-segregate with mouse mammary tumor proviruses (Mtv), Mtv-3, Mtv-6, and Mtv-13 [1].
• A congenic line of the BALB/c mouse strain with the endogenous mouse mammary tumor virus proviral gene Mtv-3: tissue-specific expression and correlation with resistance to mouse mammary tumor virus infection and tumorigenesis [2].
• We have investigated the expression of the Mtv-2 and Mtv-3 proviral genes in mouse mammary glands by examining the effect of hormones on levels of mammary tumor virus (MTV) proteins p27 (gag) and gp52 (env) in mouse mammary explants [3].
• LN hyperplasia occurred bidirectionally in LN transplantation between mice carrying Mtv-2 and Mtv-3, which are different SAg Vbeta specificity [4].

High impact information on Mtv3

• The gene was thereby not allelic to any of the previously described MMTV induction genes, Mtv-1 and Mtv-2, and is therefore called Mtv-3 [5].
• Comparison of several Mtv 3' long terminal repeat open reading frame sequences has indicated that the carboxyl terminus likely encodes the V beta specificity of these proteins [6].
• A specific Mtv-3 expression was observed in the mammary gland and spleen, but not in other lymphoid tissues, such as thymus and bone marrow [2].
• In this report we showed that a high frequency of NOD Vbeta3(+) T cells that escape deletion are activated in vivo and that this phenotype is linked to the Mtv-3 locus [7].
• T cells bearing the TCR Vbeta3 chain are disproportionately represented in the earliest stages of islet infiltration (insulitis) despite clonal deletion of most Vbeta3(+) immature thymocytes by the mammary tumor virus-3 (Mtv-3) superantigen (SAg) [7].

Biological context of Mtv3

• Analysis of TCR beta-chain V region (V beta) frequency among NOD lymphocytes reveals a profound depletion of V beta 3+ T cells, and a recent study has linked this phenomenon to the Mtv-3 insertion on chromosome 11 [8].

Anatomical context of Mtv3

• Effect of hormones on the expression of proviral genes Mtv-2 and Mtv-3 in mouse mammary gland [3].
• A strict comparison between thymus and spleen repertoires reveals no major V beta-specific deletion except the already reported V beta 3 deletion due to Mtv-3 [9].

Associations of Mtv3 with chemical compounds

• Our data indicate that the Mtv-2 locus and the Mtv-3 locus in mouse mammary gland are under separate glucocorticoid control, and that Mtv-2 expression is also stimulated by the prolactin and progesterone combination [3].

Other interactions of Mtv3

• We have examined percentages of Tcrb-V3+ T cells and Mtv integrations in [(B10 x NZB)F1 x B10.BR] mice, and show that Mtv-27 as well as Mtv-3 from NZB mice co-segregate with genes encoding deletion ligands for Tcrb-V3+ T cells without recombination [10].
• This locus consists of three parts, Mtv-3-hitchhiker-sialyltransferase, hitchhiker-sialyltransferase, and sialyltransferase alone [11].
• Co-segregation of a gene encoding a deletion ligand for Tcrb-V3+ T cells with Mtv-3 [12].
• Mtv-3 and Mtv-7 also displayed this capability [4].

References