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Cunningham C.A.,Center for Cellular and Molecular Immunology | Cunningham C.A.,Cellular One | Teixeiro E.,Center for Cellular and Molecular Immunology | Teixeiro E.,Cellular One | And 2 more authors.
Methods in Molecular Biology | Year: 2016

From the moment a developing thymocyte expresses a TCR, it is subjected to numerous interactions with self-peptide/MHC complexes that determine its ultimate fate. These include death by neglect, negative selection (apoptosis and lineage deviation), positive selection, and lineage commitment. The identification of signals that govern these unique cell fates requires the ability to assess the activity, level of expression, subcellular location, and the molecular associations of numerous proteins within the developing T cell. Thus, this chapter describes methods designed to analyze thymocyte signaling under various types of peptide-based stimulation in vitro. © Springer Science+Business Media New York 2016. Source


Cunningham C.A.,Center for Cellular and Molecular Immunology | Cunningham C.A.,Cellular One | Teixeiro E.,Center for Cellular and Molecular Immunology | Teixeiro E.,Cellular One | And 2 more authors.
Methods in Molecular Biology | Year: 2016

Potentially harmful T cell precursors are removed from the conventional T cell pool by negative selection. This process can involve the induction of apoptosis, anergy, receptor editing or deviation into a regulatory T cell lineage. As such this process is essential for the health of an organism through its contribution to central and peripheral tolerance. While a great deal is known about the process, the precise mechanisms that regulate negative selection are not clear. Furthermore, the signals that distinguish the different forms of negative selection are not fully understood. Numerous models exist with the potential to address these questions in vitro and in vivo. This chapter describes methods of fetal thymic organ culture designed to analyze the signals that determine these unique cell fates. © Springer Science+Business Media New York 2016. Source


Bodeman C.E.,Center for Cellular and Molecular Immunology | Dzierlenga A.L.,University of Arizona | Tally C.M.,Center for Cellular and Molecular Immunology | Mulligan R.M.,Center for Cellular and Molecular Immunology | And 4 more authors.
Journal of Pharmacology and Experimental Therapeutics | Year: 2013

Cholestasis results from interrupted bile flow and is associated with immune-mediated liver diseases. It is unclear how inflammation contributes to cholestasis. The aim of this study was to determine whether T and B cells contribute to hepatic transporter expression under basal and inflammatory conditions. C57BL/6J wild-type mice or strains lacking T, B, or both T and B cells were exposed to lipopolysaccharide (LPS) or saline, and livers were collected 16 hours later. Branched DNA signal amplification was used to assess mRNA levels of organic anion-transporting polypeptides (Oatp) 1a1, 1a4, and 1b2; organic cation transporter (Oct) 1; canalicular bile-salt export pump (Bsep); multidrug resistance-associated proteins (Mrp) 2 and 3; and sodium-taurocholate cotransporting polypeptide (Ntcp). Real-time polymerase chain reaction analysis was used to correlate changes of transporter expression with interleukin-1b (IL-1b), IL-6, IL-17A, IL-17F, tumor necrosis factor-α (TNF-α), and interferon-γ expression in the liver. LPS treatment inhibited Bsep and Oct1 mRNA expression, and this was abrogated with a loss of T cells, but not B cells. In addition, the absence of T cells increased Mrp2 mRNA expression, whereas B cell deficiency attenuated Oatp1a4 mRNA in LPS-treated mice. Oatp1a1, Oatp1b2, Ntcp, and Mrp3 were largely unaffected by T or B cell deficiency. Lymphocyte deficiency altered basal and inflammatory IL-6, but not TNF-α or IL-1b, mRNA expression. Taken together, these data implicate lymphocytes as regulators of basal and inflammatory hepatic transporter expression and suggest that IL-6 signaling may play a critical role. Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics. Source

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