61 research outputs found
The Victorian Newsletter (Fall 1959)
The Victorian Newsletter is edited for the English X Group of the Modern Language Association by William E. Buckler, 737 East Building, New York University, New York 3, New York.Some pages are missing from this record
The Victorian Newsletter (Fall 1978)
The Victorian Newsletter is sponsored for the Victorian Group of the Modern Language Association by the University of Florida and is published twice annually.Ironic Translation in Fifine at the Fair / Dorothy Mermin -- The Heroine of Middlemarch / Gordon S. Haight -- How Many Children had Barry Lyndon? / Winslow Rogers -- Martin Chuzzlewit: The Art of the Critical Imagination / David D. Marcus -- A New Carlyle Manuscript / Roger L. Tarr -- Disraeli's Sybil and Hollinshed's Chronicles / Lois E. Bueler -- Thackeray in Elizabeth Gaskell's The Life of Charlotte Brontë: Some Manuscript & Evidence / Angus Easson -- Dickens with a Voice like Burke's / Louie Crew -- In Defense of Margaret: Another Look at Arnold's "The Forsaken Merman" / Frank R. Giordano, Jr. -- Yeats, Tennyson, and "Innisfree" / Gary Sloan -- Victorian Group New
Nfil3/E4bp4 is required for the development and maturation of NK cells in vivo
Nuclear factor interleukin-3 (Nfil3; also known as E4-binding protein 4) is a basic region leucine zipper transcription factor that has antiapoptotic activity in vitro under conditions of growth factor withdrawal. To study the role of Nfil3 in vivo, we generated gene-targeted Nfil3-deficient (Nfil3−/−) mice. Nfil3−/− mice were born at normal Mendelian frequency and were grossly normal and fertile. Although numbers of T cells, B cells, and natural killer (NK) T cells were normal in Nfil3−/− mice, a specific disruption in NK cell development resulted in severely reduced numbers of mature NK cells in the periphery. This defect was NK cell intrinsic in nature, leading to a failure to reject MHC class I–deficient cells in vivo and reductions in both interferon γ production and cytolytic activity in vitro. Our results confirm the specific and essential requirement of Nfil3 for the development of cells of the NK lineage
Human-animal elision: a Darwinian universe in George Eliot’s novels
No abstract available
Choline acetyltransferase-expressing T cells are required to control chronic viral infection.
peer reviewedAlthough widely studied as a neurotransmitter, T cell-derived acetylcholine (ACh) has recently been reported to play an important role in regulating immunity. However, the role of lymphocyte-derived ACh in viral infection is unknown. Here, we show that the enzyme choline acetyltransferase (ChAT), which catalyzes the rate-limiting step of ACh production, is robustly induced in both CD4+ and CD8+ T cells during lymphocytic choriomeningitis virus (LCMV) infection in an IL-21-dependent manner. Deletion of Chat within the T cell compartment in mice ablated vasodilation in response to infection, impaired the migration of antiviral T cells into infected tissues, and ultimately compromised the control of chronic LCMV clone 13 infection. Our results reveal a genetic proof of function for ChAT in T cells during viral infection and identify a pathway of T cell migration that sustains antiviral immunity
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