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Myeloid antigen presenting cell populations in the murine uterus /Hudson, Sarah. January 2000 (has links) (PDF)
Thesis (Ph.D.)--University of Adelaide, Dept. of Obstetrics and Gynaecology, 2000. / Includes bibliography (leaves 217-239).
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Characterisation of non-lyphoid cells in the small intestinal lamina propria of the rat and the pigKambarage, D. M. January 1991 (has links)
No description available.
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Identification and Characterization of A Novel APC Modulating Type 2 Immunity against Influenza Virus InfectionYoo, Jae-Kwang 17 February 2011 (has links)
Herein we describe a novel APC population in mice, designated LAPCs. LAPCs are BM-derived myeloid leukocytes, distinctive from other immune cells. As APCs, LAPCs respond to various virus infections including VACV, CBV3 and influenza A virus. Notably, influenza virus-activated LAPCs capture Ag in the lungs, and migrate into the DLN and spleen with delayed kinetics compared to DCs. In the DLN, influenza virus-activated LAPCs co-localize with T cells and selectively induce Th2 effector cell polarization by cell-cell contact-mediated modulation of GATA-3 expression. In support of a role for LAPCs in anti-influenza T2 immunity, adoptive transfer experiments revealed that influenza virus-activated LAPCs selectively augmented Th2 effector T cell responses in the DLN, increased production of anti-influenza immunoglobulin (Ig) including IgE in peripheral blood and increased levels of IL-5 and eotaxin in BAL fluid in recipient influenza infected mice. LAPC recipient mice exhibited exacerbated pulmonary pathology, with delayed viral clearance and enhanced pulmonary eosinophilia. Collectively, these results highlight the importance of LAPCs as novel immuno-modulators of T2 immunity during influenza A virus infection, which is implicated in both immunoprotection and immunopathology. Subsequently, we examined the immuno-modulatory effect of type-I IFN, specifically IFN-on the immune response against pulmonary influenza virus infection. We have provided evidence that a single dose of IFN- (1×105U) augmented DC migration but inhibited LAPC migration into the DLN. mIFN- treatment skewed the immune balance toward T1 immunity, identified as enhanced T1 effector T cell responses (Th1 and CTL) but diminished T2 effector T cell responses (Th2) in influenza virus infected mice. Finally, IFN- treated mice showed accelerated viral clearance and diminished pulmonary eosinophilia in lung tissue compared to control mice. Taken together, these results suggest that anti-influenza T1 and T2 immunity may be modulated differently by DCs and LAPCs, respectively. Furthermore, these results support the therapeutic potential of type I IFNs, especially IFN-, as an alternative antiviral to control both viral replication and immunopathology induced by influenza A virus infection in humans.
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Studies of the regulatory function of L2a in mouse CD8 gene expressionYao, Xin, January 1900 (has links) (PDF)
Thesis (Ph. D.)--University of Texas at Austin, 2006. / Vita. Includes bibliographical references.
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Intracellular trafficking of invariant chain /Sevilla, Lisa M. January 2001 (has links)
Thesis (Ph. D.)--University of Chicago, Dept. of Biochemistry and Molecular Biology, 2002. / Includes bibliographical references. Also available on the Internet.
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Identification and Characterization of A Novel APC Modulating Type 2 Immunity against Influenza Virus InfectionYoo, Jae-Kwang 17 February 2011 (has links)
Herein we describe a novel APC population in mice, designated LAPCs. LAPCs are BM-derived myeloid leukocytes, distinctive from other immune cells. As APCs, LAPCs respond to various virus infections including VACV, CBV3 and influenza A virus. Notably, influenza virus-activated LAPCs capture Ag in the lungs, and migrate into the DLN and spleen with delayed kinetics compared to DCs. In the DLN, influenza virus-activated LAPCs co-localize with T cells and selectively induce Th2 effector cell polarization by cell-cell contact-mediated modulation of GATA-3 expression. In support of a role for LAPCs in anti-influenza T2 immunity, adoptive transfer experiments revealed that influenza virus-activated LAPCs selectively augmented Th2 effector T cell responses in the DLN, increased production of anti-influenza immunoglobulin (Ig) including IgE in peripheral blood and increased levels of IL-5 and eotaxin in BAL fluid in recipient influenza infected mice. LAPC recipient mice exhibited exacerbated pulmonary pathology, with delayed viral clearance and enhanced pulmonary eosinophilia. Collectively, these results highlight the importance of LAPCs as novel immuno-modulators of T2 immunity during influenza A virus infection, which is implicated in both immunoprotection and immunopathology. Subsequently, we examined the immuno-modulatory effect of type-I IFN, specifically IFN-on the immune response against pulmonary influenza virus infection. We have provided evidence that a single dose of IFN- (1×105U) augmented DC migration but inhibited LAPC migration into the DLN. mIFN- treatment skewed the immune balance toward T1 immunity, identified as enhanced T1 effector T cell responses (Th1 and CTL) but diminished T2 effector T cell responses (Th2) in influenza virus infected mice. Finally, IFN- treated mice showed accelerated viral clearance and diminished pulmonary eosinophilia in lung tissue compared to control mice. Taken together, these results suggest that anti-influenza T1 and T2 immunity may be modulated differently by DCs and LAPCs, respectively. Furthermore, these results support the therapeutic potential of type I IFNs, especially IFN-, as an alternative antiviral to control both viral replication and immunopathology induced by influenza A virus infection in humans.
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Myeloid antigen presenting cell populations in the murine uterus / Sarah Hudson.Hudson, Sarah January 2000 (has links)
Includes bibliography (leaves 217-239). / xxviii, 239 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Undertakes a detailed characterisation of the molecular phenotypes of the various antigen presenting cell populations present in the uterus, with a particular focus on the cells present at estrus, following insemination, and at the time of embryo implantation (day 4 of pregnancy). / Thesis (Ph.D.)--University of Adelaide, Dept. of Obstetrics and Gynaecology, 2000
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TLR₂-dependent modulation of antigen presenting cell functions by mycobacterial lipoproteinsPecora, Nicole Danielle. January 2008 (has links)
Thesis (Ph. D.)--Case Western Reserve University, 2008. / [School of Medicine] Department of Pathology. Includes bibliographical references.
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Direct effects of 2,3,7,8 tetrachlorodibenzo-p-dioxin on antigen-presenting cells and molecular signaling pathways in dendritic cellsRuby, Carl E. 19 November 2001 (has links)
In experimentally exposed mice, the environmental contaminant 2,3,7,8
tetrachlorodibenzo-p-dioxin (TCDD) produces significant suppression of adaptive
immune responses at low doses. However, the underlying biochemical and cellular
mechanisms of TCDD-induced immunotoxicity have remained elusive since the
identification of these effects nearly 30 years ago. Antigen-presenting cells (APC)
constitute various populations of cells essential for the initiation and maintenance of
adaptive immune responses, and represent a potential target of TCDD toxicity.
Thus, the studies presented here address the ability of TCDD to directly affect APC.
The underlying objectives of these studies focus on the investigation of molecular
signaling pathways and cellular processes potentially affected by TCDD. In order to
eliminate conflicting variables found in vivo, we used ex vivo and in vitro models to
address these objectives. Initial studies investigated the status and behavior of the
aryl hydrocarbon receptor (AhR), a transcription factor recognized as the principal
mediator of TCDD-induced immunotoxic effects, in the two main APC populations,
macrophages and dendritic cells (DC). The results demonstrated that both APC
populations expressed AhR. However, TCDD induced binding of AhR to dioxin
response elements only in macrophages, and not DC. Because TCDD has been
shown to alter DC function and survival in vivo, the possibility that TCDD altered
other signaling pathways was addressed. Specifically, activation of the transcription
factor NF-kB/Rel, integral in DC generation and function, was found to be
suppressed by TCDD. This suppression was apparently mediated by a physical
association between the AhR and proteins of NF-kB/Rel. Additional studies
demonstrated that TCDD enhances the maturation of DC and appears to sensitize
DC to apoptosis. These data establish that TCDD directly affects DC on the
molecular and cellular levels and support several potential mechanisms of TCDD-induced
immunotoxicity. / Graduation date: 2002
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A role for the transmembrane domain in the trimerization of the MHC class II-associated invariant chain /Ashman, Jonathan B. January 1999 (has links)
Thesis (Ph. D.)--University of Chicago, Committee on Immunology, June 1999. / Includes bibliographical references. Also available on the Internet.
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