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3 results on '"Mia Chandler"'

1. Disordered T cell-B cell interactions in autoantibody-positive inflammatory arthritis

Author

Amélie M. Julé, Ki Pui Lam, Maria Taylor, Kacie J. Hoyt, Kevin Wei, Maria Gutierrez-Arcelus, Siobhan M. Case, Mia Chandler, Margaret H. Chang, Ezra M. Cohen, Fatma Dedeoglu, Olha Halyabar, Jonathan Hausmann, Melissa M. Hazen, Erin Janssen, Jeffrey Lo, Mindy S. Lo, Esra Meidan, Jordan E. Roberts, Holly Wobma, Mary Beth F. Son, Robert P. Sundel, Pui Y. Lee, Peter T. Sage, Talal A. Chatila, Peter A. Nigrovic, Deepak A. Rao, and Lauren A. Henderson

Subjects
T cells, autoimmunity, autoantibodies, juvenile idiopathic arthritis, T peripheral helper cell, regulatory T (Treg) cell, Immunologic diseases. Allergy, RC581-607
Abstract

T peripheral helper (Tph) cells, identified in the synovium of adults with seropositive rheumatoid arthritis, drive B cell maturation and antibody production in non-lymphoid tissues. We sought to determine if similarly dysregulated T cell-B cell interactions underlie another form of inflammatory arthritis, juvenile oligoarthritis (oligo JIA). Clonally expanded Tph cells able to promote B cell antibody production preferentially accumulated in the synovial fluid (SF) of oligo JIA patients with antinuclear antibodies (ANA) compared to autoantibody-negative patients. Single-cell transcriptomics enabled further definition of the Tph gene signature in inflamed tissues and showed that Tph cells from ANA-positive patients upregulated genes associated with B cell help to a greater extent than patients without autoantibodies. T cells that co-expressed regulatory T and B cell-help factors were identified. The phenotype of these Tph-like Treg cells suggests an ability to restrain T cell-B cell interactions in tissues. Our findings support the central role of disordered T cell-help to B cells in autoantibody-positive arthritides.

Published
2023
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3. Preventing asthma in high risk kids (PARK) with omalizumab: Design, rationale, methods, lessons learned and adaptation

Author

Wanda Phipatanakul, David T. Mauger, Theresa W. Guilbert, Leonard B. Bacharier, Sandy Durrani, Daniel J. Jackson, Fernando D. Martinez, Anne M. Fitzpatrick, Amparito Cunningham, Susan Kunselman, Lisa M. Wheatley, Cindy Bauer, Carla M. Davis, Bob Geng, Kirsten M. Kloepfer, Craig Lapin, Andrew H. Liu, Jacqueline A. Pongracic, Stephen J. Teach, James Chmiel, Jonathan M. Gaffin, Matthew Greenhawt, Meera R. Gupta, Peggy S. Lai, Robert F. Lemanske, Wayne J. Morgan, William J. Sheehan, Jeffrey Stokes, Peter S. Thorne, Hans C. Oettgen, Elliot Israel, Lisa Bartnikas, David Kantor, Perdita Permaul, Nicole Akar-Ghibril, Mehtap Haktanir-Abul, Sigfus Gunnalaugsson, Brittany Esty, Elena Crestani, Michelle Maciag, Marissa Hauptman, Sachin N. Baxi, Elizabeth Burke-Roberts, Margee Louisias, Tina Banzon, Saddiq Habiballah, Alan Nguyen, Tregony Simoneau, Samantha Minnicozzi, Elsa Treffeisen, Brenna LaBere, Mia Chandler, Manoussa Fanny, Anna Cristina Vasquez-Muniz, Vanessa Konzelman, Giselle Garcia, Sullivan Waskosky, Anna Ramsey, Ethan Ansel-Kelly, Elizabeth Fitzpatrick, Vaia Bairaktaris, Jesse Fernandez, Brianna Hollister, Owen Lewis, Masai McIntosh, Sigrid Almeida, Carolyn Kercsmar, Karen McDowell, Cassie Shipp, Stephanie (Logsdon) Ward, Nancy Lin, Alisha George, Ryne Simpson, Ina St. Onge, Will Corwin, Grant Geigle, Alisha Hartmann, John Broderick, Stanley Szefler, Naomi Miyazawa, Brooke Tippin, Darci Anderson, Sonya Belimezova, Nidhya Navanandan, Tanya Watson, Michelle Olson, Wanda Caldwell, Caroline Horner, Lila Kertz, Tina Norris, Katherine Rivera-Spoljaric, Andrea Coverstone, Molly McDowell, Sarah Laughlin, Gina Laury, Rosanne Donato, Elizabeth Beckett-Firmage, Elia A. Cornidez, Silvia Lopez, Michele Simon, Raymond Skeps, Monica Vasquez, Rob Gage, Heather Shearer, Melissa Pecak, Sandi Winters, Christine Rukasin, Bernadette McNally, Darcy Johnson, Brian Vickery, Jocelyn Grunwell, Morgan Nicholls, Taqwa El-Hussein, Shilpa Patel, Dinsesh Pillai, Melanie Makhija, Rachel Robison, Jennifer Bosworth, Michelle Catalano, Kathleen Cassin, Laura Bamaca DeLeon, Nicole Titus, Sydney Leibel, Seema Aceves, Diba Mortazavi, Lauren Loop, Sara Anvari, Aikaterini Anagnostou, Kathy Pitts, Sopar Sebutra, Daisy Tran, Chivon McMullen-Jackson, Jay Jin, Nadia Krupp, Clement Ren, Girish Vitalpur, Lori Shively, Patrick Campbell, Lisa Bendy, Lisa France, Sylvia Jara, Sarah Cichy, Linda Engle, Aimee Merchlinski, Melanie Payton, Pam Ramsey, James Schmidt, Dan Tekely, Angela Updegrave, Rachel Weber, Ronald Zimmerman, Nervana Metwali, Xuefang Jing, Melissa Walker, Steven S. Sigelman, Ling Li, and Sanaz Hamrah

Subjects
Allergy, Omalizumab, medicine.disease_cause, Immunoglobulin E, Antibodies, Monoclonal, Humanized, Article, 03 medical and health sciences, 0302 clinical medicine, Immune system, immune system diseases, medicine, Humans, Pharmacology (medical), 030212 general & internal medicine, Anti-Asthmatic Agents, Risk factor, Child, Sensitization, Asthma, 030505 public health, biology, business.industry, Antibodies, Monoclonal, General Medicine, medicine.disease, respiratory tract diseases, medicine.anatomical_structure, Immunology, biology.protein, Rhinovirus, 0305 other medical science, business, medicine.drug
Abstract

Asthma remains one of the most important challenges to pediatric public health in the US. A large majority of children with persistent and chronic asthma demonstrate aeroallergen sensitization, which remains a pivotal risk factor associated with the development of persistent, progressive asthma throughout life. In individuals with a tendency toward Type 2 inflammation, sensitization and exposure to high concentrations of offending allergens is associated with increased risk for development of, and impairment from, asthma. The cascade of biological responses to allergens is primarily mediated through IgE antibodies and their production is further stimulated by IgE responses to antigen exposure. In addition, circulating IgE impairs innate anti-viral immune responses. The latter effect could magnify the effects of another early life exposure associated with increased risk of the development of asthma – viral infections. Omalizumab binds to circulating IgE and thus ablates antigen signaling through IgE-related mechanisms. Further, it has been shown restore IFN-α response to rhinovirus and to reduce asthma exacerbations during the viral season. We therefore hypothesized that early blockade of IgE and IgE mediated responses with omalizumab would prevent the development and reduce the severity of asthma in those at high risk for developing asthma. Herein, we describe a double-blind, placebo-controlled trial of omalizumab in 2–3 year old children at high risk for development of asthma to prevent the development and reduce the severity of asthma. We describe the rationale, methods, and lessons learned in implementing this potentially transformative trial aimed at prevention of asthma.

Published
2020

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