Mnt is a Max-interacting protein that can antagonize the activities of @entity18122 oncoproteins in cultured cells. Mnt null @entity19 die soon after birth, but conditional deletion of Mnt in breast epithelium leads to @entity5 formation. These and related data suggest that Mnt functions as a @entity5 suppressor. Here we show that conditional deletion of Mnt in T cells leads to @entity5 formation but also causes @entity32 . Deletion of Mnt caused increased apoptosis of thymic T cells and interfered with T-cell development yet led to spleen, liver, and @entity1600 . The proportion of T cells in the spleen and lymph nodes was reduced, and the numbers of cells in non-T-cell immune cell populations were elevated. The disruption of immune homeostasis is linked to a strong skewing toward production of T-helper 1 (Th1) cytokines and enhanced proliferation of activated Mnt-deficient CD4+ T cells. Consistent with Th1 polarization in vivo, extensive @entity32 and liver @entity39 developed. Finally, most @entity19 lacking Mnt in T cells ultimately succumbed to @entity784 . These results strengthen the argument that Mnt functions as a @entity5 suppressor and reveal a critical and surprising role for Mnt in the regulation of T-cell development and in T-cell-dependent immune homeostasis.

@entity32 and lymphomagenesis caused by deletion of the XXXX antagonist Mnt in T cells.

@entity32 :: ('MESH:D007249', 'Disease') :: ['inflammatory disease', 'intestinal inflammation'] @entity18122 :: ('17869(Tax:10090)', 'Gene') :: ['Myc'] @entity39 :: ('MESH:D009336', 'Disease') :: ['necrosis'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity784 :: ('MESH:D016399', 'Disease') :: ['T-cell lymphoma'] @entity1600 :: ('MESH:D014388', 'Disease') :: ['lymph node enlargement']
@entity18122 :: (17869(Tax:10090),Gene) :: ['Myc']
