Publications
38 results found
Roberts EW, Deonarine A, Jones JO, et al., 2013, Depletion of stromal cells expressing fibroblast activation protein-alpha from skeletal muscle and bone marrow results in cachexia and anemia, Journal of Experimental Medicine, Vol: 210, Pages: 1137-1151, ISSN: 0022-1007
Fibroblast activation protein-α (FAP) identifies stromal cells of mesenchymal origin in human cancers and chronic inflammatory lesions. In mouse models of cancer, they have been shown to be immune suppressive, but studies of their occurrence and function in normal tissues have been limited. With a transgenic mouse line permitting the bioluminescent imaging of FAP+ cells, we find that they reside in most tissues of the adult mouse. FAP+ cells from three sites, skeletal muscle, adipose tissue, and pancreas, have highly similar transcriptomes, suggesting a shared lineage. FAP+ cells of skeletal muscle are the major local source of follistatin, and in bone marrow they express Cxcl12 and KitL. Experimental ablation of these cells causes loss of muscle mass and a reduction of B-lymphopoiesis and erythropoiesis, revealing their essential functions in maintaining normal muscle mass and hematopoiesis, respectively. Remarkably, these cells are altered at these sites in transplantable and spontaneous mouse models of cancer-induced cachexia and anemia. Thus, the FAP+ stromal cell may have roles in two adverse consequences of cancer: their acquisition by tumors may cause failure of immunosurveillance, and their alteration in normal tissues contributes to the paraneoplastic syndromes of cachexia and anemia.
Russ BE, Denton AE, Hatton L, et al., 2012, Defining the molecular blueprint that drives CD8(+) T cell differentiation in response to infection, Frontiers in Immunology, Vol: 3, ISSN: 1664-3224
A cardinal feature of adaptive, cytotoxic T lymphocyte (CTL)-mediated immunity is the ability of naïve CTLs to undergo a program of differentiation and proliferation upon activation resulting in the acquisition of lineage-specific T cell functions and eventual establishment of immunological memory. In this review, we examine the molecular factors that shape both the acquisition and maintenance of lineage-specific effector function in virus-specific CTL during both the effector and memory phases of immunity.
Denton AE, Wesselingh R, Gras S, et al., 2011, Affinity Thresholds for Naive CD8<SUP>+</SUP> CTL Activation by Peptides and Engineered Influenza A Viruses, JOURNAL OF IMMUNOLOGY, Vol: 187, Pages: 5733-5744, ISSN: 0022-1767
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- Citations: 41
Denton AE, Russ BE, Doherty PC, et al., 2011, Differentiation-dependent functional and epigenetic landscapes for cytokine genes in virus-specific CD8<SUP>+</SUP> T cells, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 108, Pages: 15306-15311, ISSN: 0027-8424
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- Citations: 67
Croom HA, Denton AE, Valkenburg SA, et al., 2011, Memory precursor phenotype of CD8<SUP>+</SUP> T cells reflects early antigenic experience rather than memory numbers in a model of localized acute influenza infection, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 41, Pages: 682-693, ISSN: 0014-2980
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- Citations: 19
Juelich T, Sutcliffe EL, Denton A, et al., 2010, Interplay between chromatin remodeling and epigenetic changes during lineage-specific commitment to granzyme B expression (vol 183, pg 7063, 2009), JOURNAL OF IMMUNOLOGY, Vol: 184, Pages: 1653-1653, ISSN: 0022-1767
Juelich T, Sutcliffe E, Denton A, et al., 2009, Interplay between Chromatin Remodeling and Epigenetic Changes during Lineage-Specific Commitment to Granzyme B Expression, JOURNAL OF IMMUNOLOGY, Vol: 183, Pages: 7063-7072, ISSN: 0022-1767
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- Citations: 36
Denton AE, Doherty PC, Turner SJ, et al., 2007, IL-18, but not IL-12, is required for optimal cytokine production by influenza virus-specific CD8<SUP>+</SUP> T cells, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 37, Pages: 368-375, ISSN: 0014-2980
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- Citations: 46
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