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3 results on '"Michelle Bolner"'

1. Canadian Society of Allergy and Clinical Immunology annual scientific meeting 2016

Author

Mohammad A. Alsayegh, Hanan Alshamali, Mousa Khadada, Amanda Ciccolini, Anne K. Ellis, Diana Quint, William Powley, Laurie Lee, Yahya Fiteih, Shairaz Baksh, Harissios Vliagoftis, Sebastien K. Gerega, Brad Millson, Katia Charland, Stephane Barakat, Xichun Sun, Ricardo Jimenez, Susan Waserman, Mark J. FitzGerald, Jacques Hébert, Josiane Cognet-Sicé, Kevin E. Renahan, Saiful Huq, Rishma Chooniedass, Scott Sawyer, Hans Pasterkamp, Allan Becker, Steven G. Smith, Shiyuan Zhang, Kavisha Jayasundara, Claire Tacon, Alex Simidchiev, Gilbert Nadeau, Necdet Gunsoy, Hana Mullerova, Frank Albers, Young Woong Kim, Casey P. Shannon, Amrit Singh, Helen Neighbour, Mark Larché, Scott J. Tebbutt, Annika Klopp, Lorena Vehling, Allan B. Becker, Padmaja Subbarao, Piushkumar J. Mandhane, Stuart E. Turvey, Malcolm R. Sears, Meghan B. Azad, and the Canadian Healthy Infant Longitudinal Development Study Investigators, Keely Loewen, Barret Monchka, Salaheddin M. Mahmud, Geert ‘t Jong, Cristina Longo, Gillian Bartlett, Francine M. Ducharme, Tibor Schuster, Brenda MacGibbon, Tracie Barnett, Michelle L. North, Jeff Brook, Elizabeth Lee, Vanessa Omana, Jenny Thiele, Lisa M. Steacy, Greg Evans, Miriam Diamond, Gordon L. Sussman, Yann Amistani, Kathy Abiteboul, Mark W. Tenn, ChenXi Yang, Christopher Carlsten, Edward M. Conway, Douglas Mack, Yasmin Othman, Colin M. Barber, Chrystyna Kalicinsky, Andrea E. Burke, Mary Messieh, Parameswaran Nair, Chun T. Che, Lindsay Douglas, Joel Liem, Lucy Duan, Charlotte Miller, Pascale Dupuis, Lori A. Connors, Michael N. Fein, Joseph Shuster, Hani Hadi, Brooke Polk, Nikita Raje, Roxane Labrosse, Philippe Bégin, Louis Paradis, Anne Des Roches, Jonathan Lacombe-Barrios, Sanju Mishra, Gina Lacuesta, Meredith Chiasson, Babar Haroon, Kara Robertson, Thomas Issekutz, Desmond Leddin, Stephen Couban, Lori Connors, Adrienne Roos, Amin Kanani, Edmond S. Chan, Robert Schellenberg, Lana Rosenfield, Anna Cvetkovic, Kevin Woodward, Jaclyn Quirt, Wade T. A. Watson, Edson Castilho, Jennifer A. Sullivan, Beverley Temple, Donna Martin, Victoria E. Cook, Christopher Mills, Elodie Portales-Casamar, Lisa W. Fu, Alexander Ho, Jeffrey Zaltzman, Lucy Chen, Peter Vadas, Sofianne Gabrielli, Ann Clarke, Harley Eisman, Judy Morris, Lawrence Joseph, Sebastien LaVieille, Moshe Ben-Shoshan, François Graham, Charles Barnes, Jay Portnoy, Vincent Stagg, Elinor Simons, Diana Lefebvre, David Dai, Piushkumar Mandhane, Malcolm Sears, Herman Tam, F. Estelle R. Simons, Dhaifallah Alotaibi, Bassel Dawod, Matthew C. Tunis, Jean Marshall, Marylin Desjardins, Marianne Béland, Duncan Lejtenyi, Jean-Phillipe Drolet, Martine Lemire, Christos Tsoukas, Francisco J.D. Noya, Reza Alizadehfar, Christine T. McCusker, Bruce D. Mazer, Danay Maestre-Batlle, Evelyn Gunawan, Christopher F. Rider, Anette K. Bølling, Olga M. Pena, Daniel Suez, Isaac Melamed, Iftikhar Hussain, Mark Stein, Sudhir Gupta, Kenneth Paris, Sandor Fritsch, Christelle Bourgeois, Heinz Leibl, Barbara McCoy, Martin Noel, Leman Yel, Ori Scott, Brenda Reid, Adelle Atkinson, Vy Hong-Diep Kim, Chaim M. Roifman, Eyal Grunebaum, Eiman AlSelahi, Fernando Aleman, Amber Oberle, Mike Trus, Gordon Sussman, Amin S. Kanani, Olivier Chambenoi, Sima Chiva-Razavi, Savannah Grodecki, Nikhil Joshi, Peter Menikefs, David Holt, Teresa Pun, Damian Tworek, Raphael Hanna, Delia Heroux, Elli Rosenberg, Leah Stiemsma, Stuart Turvey, Judah Denburg, Christopher Mill, Timothy Teoh, Preeti Zimmer, Vishal Avinashi, Mihaela Paina, Ahmed A. Darwish Hassan, John Paul Oliveria, Chris Olesovsky, Gail Gauvreau, Linda Pedder, Paul K. Keith, Greg Plunkett, Michelle Bolner, Persia Pourshahnazari, Donald Stark, Kateryna Vostretsova, Andrew Moses, Andrew Wakeman, Alexander Singer, Thomas Gerstner, Elissa Abrams, Sara F. Johnson, and Roberta L. Woodgate

Subjects
Asthma, Food Allergy, Allergic Rhinitis, Chronic Granulomatous Disease, Immunologic diseases. Allergy, RC581-607
Published
2017
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2. Stat3 Signaling Promotes Survival And Maintenance Of Medullary Thymic Epithelial Cells.

Author

Dakshayani Lomada, Manju Jain, Michelle Bolner, Kaitlin A G Reeh, Rhea Kang, Madhava C Reddy, John DiGiovanni, and Ellen R Richie

Subjects
Genetics, QH426-470
Abstract

Medullary thymic epithelial cells (mTECs) are essential for establishing central tolerance by expressing a diverse array of self-peptides that delete autoreactive thymocytes and/or divert thymocytes into the regulatory T cell lineage. Activation of the NFκB signaling pathway in mTEC precursors is indispensable for mTEC maturation and proliferation resulting in proper medullary region formation. Here we show that the Stat3-mediated signaling pathway also plays a key role in mTEC development and homeostasis. Expression of a constitutively active Stat3 transgene targeted to the mTEC compartment increases mTEC cellularity and bypasses the requirement for signals from positively selected thymocytes to drive medullary region formation. Conversely, conditional deletion of Stat3 disrupts medullary region architecture and reduces the number of mTECs. Stat3 signaling does not affect mTEC proliferation, but rather promotes survival of immature MHCIIloCD80lo mTEC precursors. In contrast to striking alterations in the mTEC compartment, neither enforced expression nor deletion of Stat3 affects cTEC cellularity or organization. These results demonstrate that in addition to the NFkB pathway, Stat3-mediated signals play an essential role in regulating mTEC cellularity and medullary region homeostasis.

Published
2016
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3. Stat3 Signaling Promotes Survival And Maintenance Of Medullary Thymic Epithelial Cells

Author

Madhava C. Reddy, Dakshayani Lomada, John DiGiovanni, Ellen R. Richie, Rhea Kang, Michelle Bolner, Manju Jain, and Kaitlin A. G. Reeh

Subjects
0301 basic medicine, STAT3 Transcription Factor, Cancer Research, lcsh:QH426-470, Regulatory T cell, Cellular differentiation, Transgene, T-Lymphocytes, Embryonic Development, Thymus Gland, Biology, Lymphocyte Activation, 03 medical and health sciences, Mice, Genetics, medicine, Compartment (development), Animals, Transgenes, CD40 Antigens, STAT3, Molecular Biology, Genetics (clinical), Ecology, Evolution, Behavior and Systematics, Thymocytes, NF-kappa B, Gene Expression Regulation, Developmental, Cell Differentiation, Epithelial Cells, NFKB1, Flow Cytometry, Cell biology, lcsh:Genetics, 030104 developmental biology, medicine.anatomical_structure, biology.protein, Signal transduction, Central tolerance, Research Article, Signal Transduction
Abstract

Medullary thymic epithelial cells (mTECs) are essential for establishing central tolerance by expressing a diverse array of self-peptides that delete autoreactive thymocytes and/or divert thymocytes into the regulatory T cell lineage. Activation of the NFκB signaling pathway in mTEC precursors is indispensable for mTEC maturation and proliferation resulting in proper medullary region formation. Here we show that the Stat3-mediated signaling pathway also plays a key role in mTEC development and homeostasis. Expression of a constitutively active Stat3 transgene targeted to the mTEC compartment increases mTEC cellularity and bypasses the requirement for signals from positively selected thymocytes to drive medullary region formation. Conversely, conditional deletion of Stat3 disrupts medullary region architecture and reduces the number of mTECs. Stat3 signaling does not affect mTEC proliferation, but rather promotes survival of immature MHCIIloCD80lo mTEC precursors. In contrast to striking alterations in the mTEC compartment, neither enforced expression nor deletion of Stat3 affects cTEC cellularity or organization. These results demonstrate that in addition to the NFkB pathway, Stat3-mediated signals play an essential role in regulating mTEC cellularity and medullary region homeostasis., Author Summary T cells, an essential component of the immune system, generate protective immune responses against pathogenic organisms and cancer cells. T cells are produced in the thymus, which provides a unique microenvironment required for T cell development. Distinct subsets of thymic epithelial cells (TECs) in the outer cortex and inner medulla provide signals required for the survival and differentiation of immature T cells, referred to as thymocytes. Medullary TECs (mTECs) play a critical role in preventing autoimmunity because they have the unique ability to express peptides found in other organs throughout the body. Presentation of self-peptides to thymocytes causes deletion of cells that express high affinity self-reactive receptors. Numerous studies have established that a major signaling pathway mediated by NFκB family members is indispensable for mTEC development. However, whether other signaling pathways are also required has remained an open question. Here, we use gain- and loss-of-function genetic approaches to demonstrate that another pathway, mediated by Stat3 signaling, plays an important role in mTEC development and homeostasis. We show that constitutive Stat3 activation enhances the survival of immature mTECs and bypasses the requirement for thymocyte-derived signals in medullary region formation. In contrast, Stat3 depletion reduces mTEC cellularity and impairs medullary region formation.

Published
2016

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