Abstract Supplement FOCIS 2017 1 Federation of Clinical Immunology Societies June 14-17, 2017 Chicago, Illinois FOCIS 2017 Abstract Supplement TABLE OF CONTENTS Abstracts by Subject Area ............................................................................................................................. 2 Allergy/asthma........................................................................................................................................... 2 Autoimmune neurologic diseases .............................................................................................................. 3 Autoimmune rheumatologic diseases ...................................................................................................... 11 Bone marrow or stem cell transplantation ............................................................................................... 32 Cytokines/chemokines ............................................................................................................................ 34 Diabetes and other autoimmune endocrine diseases .............................................................................. 36 Genetics .................................................................................................................................................. 55 Immune monitoring .................................................................................................................................. 59 Immunity & infection ................................................................................................................................ 64 Immunodeficiency: primary or acquired ................................................................................................... 83 Immuno-dermatology .............................................................................................................................. 91 Immunology of the eye ............................................................................................................................ 93 Immuno-oncology .................................................................................................................................... 94 Inflammatory bowel diseases ................................................................................................................ 106 Innate immunity ..................................................................................................................................... 112 Organ transplantation ............................................................................................................................ 116 Other ..................................................................................................................................................... 118 Reproductive immunology ..................................................................................................................... 120 Therapeutics/pharmacology .................................................................................................................. 121 Transplantation...................................................................................................................................... 127 Abstract Index by Subject Area ................................................................................................................. 132 Abstract Index by FOCIS Pillar .................................................................................................................. 133 Abstract Index by Author ........................................................................................................................... 134 1 ABSTRACTS BY SUBJECT AREA Allergy/asthma T.64. Immune Memory is Established at the Incipient, Preclinical Stages of Food Allergy Roopali Chaudhary, Rodrigo Jiménez-Saiz, Joshua Koenig, Alexandra Florescu, Tina Walker-Fattouh, Talveer S. Mandur, Kelly Bruton, Melissa E. Gordon, Yosef Ellenbogen, Paul Spill, Susan Waserman and Manel Jordana. McMaster University, Hamilton, ON, Canada Most patients with food allergy experience clinical symptoms at their first known exposure. A pre-requisite for the expression of such symptoms is the development of allergen-specific IgE that facilitates mast cell and basophil degranulation upon subsequent allergen exposure. Here, we searched for immunological events that might precede the generation of allergen-specific IgE. As these potential events are silent, we used a murine system. Mice were orally exposed only once to a food allergen (peanut or ovalbumin) with cholera toxin (CT), a classical Th2 adjuvant. Under these conditions, mice lacked allergen-specific germinal centres in the lamina propria (LP) of the small intestine and mesenteric lymph nodes (mLNs). They also had undetectable levels of allergen-specific IgE in serum and allergen-specific plasma cells in the bone marrow. Accordingly, these mice did not experience anaphylaxis on systemic allergen challenge. However, we detected allergen-specific IgG1+ B cells in LP, spleen and mLNs by flow cytometry. In addition, stimulation of splenocytes with allergen in vitro induced CD4+ T-cell proliferation and Th2-associated cytokine secretion. When these mice were orally re-exposed to allergen without adjuvant, they developed allergen-specific IgE and underwent anaphylaxis on systemic challenge, even when allergen re-exposures were done 9 months after the initial, single exposure to allergen + CT. These findings indicate that long-lived allergen-specific memory is established after a single, clinically and humorally silent, immunogenic exposure to allergen, which is activated by inherently innocuous allergen exposures. These findings encourage further research to identify tools for the early prediction of food allergy. T.65. GSDMB, a Gene Located in the 17q21 Asthma-susceptibility Locus Induces an Asthma Phenotype Mediated by Airway Remodeling Without Lung Inflammation Sudipta Das, Marina Miller and David Broide University of California, San Diego, La Jolla, CA BACKGROUND: Chromosome 17q21 contains a cluster of genes that may either individually, or in combination, be responsible for its strong genetic linkage to asthma. In this study, we focused on GSDMB as its biological function in asthma is unknown. METHODS: GSDMB expression was evaluated in human lung sections from asthmatic patients and normal individuals. As the SNP linking chromosome 17q21 to asthma is associated with increased GSDMB expression, we generated transgenic mice expressing increased levels of the human GSDMB transgene (hGSDMBZp3-Cre). The levels of Th2 cytokines, remodeling genes and chemokines were assessed by qPCR, immunohistochemistry and ELISA. RESULTS: We identified that GSDMB is highly expressed in lung bronchial epithelium in human asthma. Overexpression of GSDMB in primary human bronchial epithelium increased the expression of genes important to both airway remodeling (TGF-β1, 5-LO) and airway-hyperresponsiveness (AHR) (5-LO). Interestingly, unchallenged hGSDMBZp3-Cre mice showed a significant spontaneous increase in airway remodeling, with increased smooth muscle mass and increased fibrosis as early as 8 weeks of age, which persisted until 24 weeks of age. In addition, hGSDMBZp3-Cre mice also showed a significant 2 spontaneous increase in AHR in the absence of airway inflammation, with increases in the same remodeling and AHR mediators (TGF-β1, 5-LO) observed in vitro in GSDMB-overexpressing epithelial cells. CONCLUSION: Our studies demonstrate that GSDMB, a gene highly linked to asthma but whose function in asthma is previously unknown, regulates AHR and airway remodeling without airway inflammation through a previously unrecognized pathway in which GSDMB induces 5-LO to induce TGF-β1 in bronchial epithelium. T.66. Gabapentin Therapy for Biphasic Anaphylaxis Karen Quan1, Helene Pham1, Bowei Su1 and Raffi Tachdjian2 1AIRE Medical of Los Angeles, Santa Monica, CA, 2Univeristy of California, Los Angeles, Santa Monica, CA Idiopathic Anaphylaxis is a constellation of symptoms that include one or more of the following: angioedema, urticaria, gastrointestinal abnormalities, and decreased blood pressure without any recognized external trigger. Gabapentin, an anticonvulsant drug, has been used in different conditions associated with chronic neuropathic pain and pruritic disorders. Because neuropathic pain and pruritus share similar pathogenic mechanisms, neuropathic analgesics like gabapentin have been shown to be effective therapeutic options. We present a 29-year-old female patient with biphasic idiopathic anaphylactic reactions, with accompanying angioedema, urticaria, severe abdominal pain, and diarrhea. The angioedema attacks occurred in laryngeal, facial, and upper extremity regions. Her lab results show normal complement, tryptase levels, and stool culture, and bone marrow biopsy was negative for systemic mastocytosis. Frequency of attacks ranged from 1 to over 20 times a day. Frequency and unpredictability of attacks prompted her to switch to a liquid elemental diet. She was unresponsive to cromoglicic acid, extended-release morphine, hydromorphone, and fentanyl, and only responded to IM/IV epinephrine during the attacks. We placed the patient on gabapentin 300 mg 4 times daily and within 2 days, she reported 90% resolution of gastrointestinal pain, and returned to a normal diet without anaphylactic episodes. Gabapentin therapy appears to have been beneficial in the treatment of idiopathic anaphylaxis,