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Purpose In vivo immune cell tracking using MRI is a valuable tool for studying the mechanisms underlying successful cancer therapies. Current cell labeling methods using superparamagnetic iron oxide (SPIO) lack the specificity and persistence needed to track the fate and location of transplanted cells long-term. Magnetospirillium magneticum is a commercially available, iron-producing bacterium that can be taken up by, and live harmoniously within, mammalian cells as magneto-endosymbionts (MEs). MEs have shown promise as labeling agents for in vivo stem and cancer cell tracking but have yet to be evaluated in immune cells. This pilot study examined ME labeling in myeloid-derived suppressor cells (MDSCs), cytotoxic T lymphocytes (CTLs) and dendritic cells (DCs) and its effects on cell purity, function and MRI contrast. Procedures: MDSCs, CTLs and DCs were incubated with MEs at various ME labelling ratios (MLR) and various biological metrics and iron uptake were assessed. For in vivo imaging, MDSCs were labeled overnight with either MEs or SPIO (Molday ION Rhodamine B) and injected into C3 tumor-bearing mice via tail vein injection 24 days post-implant and scanned daily with MRI for one week to assess cellular quantification. Results Following incubations MDSCs contained 0.62 and 2.22 pg Fe/ cell. CTLs achieved Fe loading of In vivo data demonstrated that the MDSCs labeled with MEs generated sufficient contrast to be detectable using TurboSPI, similar to SPIO-labeled cells. Conclusions Cells can be labeled with pre-clinically relevant amounts of MEs without compromising cell viability. Care must be taken at higher concentrations of MEs, which may affect the functional activity and/or morphology of some cell types. Immune cells with minimal phagocytic behaviour have much lower iron content per cells after incubation with MEs vs SPIO; however, MEs can successfully be used as a contrast agent for phagocytic immune cells.

Purpose of review Breastfeeding provides passive immunity while the neonatal immune system matures, and may also protect against chronic immune-mediated conditions long after weaning. This review summarizes current knowledge and new discoveries about human milk and mucosal immunity. Recent findings New data suggest that certain microbes in maternal milk may seed and shape the infant gut microbiota, which play a key role in regulating gut barrier integrity and training the developing immune system. Human milk oligosaccharides, best known for their prebiotic functions, have now been shown to directly modulate gene expression in mast and goblet cells in the gastrointestinal tract. Epidemiologic data show a reduced risk of peanut sensitization among infants breastfed by peanut-consuming mothers, suggesting a role for milk-borne food antigens in tolerance development. Cross-fostering experiments in mice suggest the soluble Toll-like receptor 2, found in human milk, may be critical in this process. Finally, interest in human milk antibodies surged during the pandemic with the identification of neutralizing severe acute respiratory syndrome coronavirus 2 antibodies in maternal milk following both natural infection and vaccination. Summary Human milk provides critical immune protection and stimulation to breastfed infants. Understanding the underlying mechanisms could identify new therapeutic targets and strategies for disease prevention across the lifespan.

Breastfeeding provides passive immunity while the neonatal immune system matures, and may also protect against chronic immune-mediated conditions long after weaning. This review summarizes current knowledge and new discoveries about human milk and mucosal immunity.New data suggest that certain microbes in maternal milk may seed and shape the infant gut microbiota, which play a key role in regulating gut barrier integrity and training the developing immune system. Human milk oligosaccharides, best known for their prebiotic functions, have now been shown to directly modulate gene expression in mast and goblet cells in the gastrointestinal tract. Epidemiologic data show a reduced risk of peanut sensitization among infants breastfed by peanut-consuming mothers, suggesting a role for milk-borne food antigens in tolerance development. Cross-fostering experiments in mice suggest the soluble Toll-like receptor 2, found in human milk, may be critical in this process. Finally, interest in human milk antibodies surged during the pandemic with the identification of neutralizing severe acute respiratory syndrome coronavirus 2 antibodies in maternal milk following both natural infection and vaccination.Human milk provides critical immune protection and stimulation to breastfed infants. Understanding the underlying mechanisms could identify new therapeutic targets and strategies for disease prevention across the lifespan.

Voltage gated sodium (Nav) channels contribute to axonal damage following demyelination in experimental autoimmune encephalomyelitis (EAE), a rodent model of multiple sclerosis (MS). The Nav1.6 isoform has been implicated as a primary contributor in this process. However, the role of Nav1.6 in immune processes, critical to the pathology of both MS and EAE, has not been extensively studied. EAE was induced with myelin oligodendrocyte (MOG35-55) peptide in Scn8admu/+ mice, which have reduced Nav1.6 levels. Scn8admu/+ mice demonstrated improved motor capacity during the recovery and early chronic phases of EAE relative to wild-type animals. In the optic nerve, myeloid cell infiltration and the effects of EAE on the axonal ultrastructure were also significantly reduced in Scn8admu/+ mice. Analysis of innate immune parameters revealed reduced plasma IL-6 levels and decreased percentages of Gr-1high/CD11b+ and Gr-1int/CD11b+ myeloid cells in the blood during the chronic phase of EAE in Scn8admu/+ mice. Elevated levels of the anti-inflammatory cytokines IL-10, IL-13, and TGF-β1 were also observed in the brains of untreated Scn8admu/+ mice. A lipopolysaccharide (LPS) model was used to further evaluate inflammatory responses. Scn8admu/+ mice displayed reduced inflammation in response to LPS challenge. To further evaluate if this was an immune cell-intrinsic difference or the result of changes in the immune or hormonal environment, mast cells were derived from the bone marrow of Scn8admu/+ mice. These mast cells also produced lower levels of IL-6, in response to LPS, compared with those from wild type mice. Our results demonstrate that in addition to its recognized impact on axonal damage, Nav1.6 impacts multiple aspects of the innate inflammatory response.

Triple-negative breast cancer (TNBC) is an invasive subtype of breast cancer but paradoxically associated with increased tumor-infiltrating leukocytes. The molecular and cellular mechanisms underlying TNBC immunobiology are incompletely understood. Interleukin (IL)-17A is a pro-inflammatory cytokine that has both pro- and anti-tumor effects and found in 40–80% of TNBC samples. We report here that IL-17A mRNA and protein are detectable in some human TNBC cell lines and further upregulated by IL-23 and LPS stimulation. Furthermore, the impact of tumor-derived IL-17A in host immune response and tumor growth was examined using murine TNBC 4T1 mammary carcinoma cells transduced with an adenoviral vector expressing IL-17A (AdIL-17A) or control vector (Addl). Compared to Addl-transduction, AdIL-17A-transduction enhanced 4T1 tumor growth and lung metastasis in vivo, which was associated with a marked expansion of myeloid-derived suppressor cells (MDSCs). However, AdIL-17A-transduction also induced strong organ-specific and time-dependent immune activation indicated by dynamic changes of NK cells, B cells, CD4, and CD8 T cells in peripheral blood, lung, and tumor site, as well as the plasma levels of IFNγ. Such findings highlight that tumor-associated IL-17A induces concurrent immune activation and immune suppression. Administration of anti-Gr1 or anti-G-CSF antibody effectively depleted MDSCs in vivo, markedly reducing the growth of AdIL-17A-transduced 4T1 tumors, and eliminating lung metastasis. Collectively, our study demonstrates that MDSC depletion is an effective and practical approach for treating IL-17A-enriched mammary carcinomas.

Background The role of breast-feeding in the development of oral tolerance and allergic diseases is controversial, which could be related to variability in milk components. Toll-like receptor 2 (TLR2) is an innate immune receptor implicated in regulating allergic disease development. Objectives We examined whether deficiency of maternal TLR2 affects the normal development of oral tolerance and related immune parameters during lactation in a mouse model. Methods Heterozygous TLR2+/– pups from wild-type (WT) or TLR2–/– dams were fed either by their biologic dam or a dam of the alternate genotype. Development of oral tolerance to ovalbumin, levels of tolerogenic CD103+ dendritic cells, and regulatory T (Treg) cells, as well as intestinal permeability, were evaluated in these pups. The levels of key immune mediators in milk from TLR2–/– and WT mothers were also examined. Results Heterozygous TLR2+/– pups that were born to and nursed by TLR2–/– dams exhibited impaired oral tolerance. This was prevented by cross-fostering onto WT (TLR2+/+) dams. Impairments included selective elevation in anti-ovalbumin IgE in plasma following immunization, reduced numbers of tolerogenic dendritic cells and Treg cells in the intestinal tract, and increased intestinal permeability. TLR2 deficiency also affected milk content of insulin-like growth factor-1, IFN-γ, IL-6, and IL-13. Conclusion Our results underline a critical role for TLR2 in regulating milk components that are essential for development of oral tolerance in early life and demonstrate the importance of considering the immune status of nursing mothers in studies of immune development and responses.

Background In multiple sclerosis (MS) and in the experimental autoimmune encephalomyelitis (EAE) model of MS, the Nav1.6 voltage-gated sodium (Nav) channel isoform has been implicated as a primary contributor to axonal degeneration. Following demyelination Nav1.6, which is normally co-localized with the Na+/Ca2+ exchanger (NCX) at the nodes of Ranvier, associates with β-APP, a marker of neural injury. The persistent influx of sodium through Nav1.6 is believed to reverse the function of NCX, resulting in an increased influx of damaging Ca2+ ions. However, direct evidence for the role of Nav1.6 in axonal degeneration is lacking. Methods In mice floxed for Scn8a, the gene that encodes the α subunit of Nav1.6, subjected to EAE we examined the effect of eliminating Nav1.6 from retinal ganglion cells (RGC) in one eye using an AAV vector harboring Cre and GFP, while using the contralateral either injected with AAV vector harboring GFP alone or non-targeted eye as control. Results In retinas, the expression of Rbpms, a marker for retinal ganglion cells, was found to be inversely correlated to the expression of Scn8a. Furthermore, the gene expression of the pro-inflammatory cytokines Il6 (IL-6) and Ifng (IFN-γ), and of the reactive gliosis marker Gfap (GFAP) were found to be reduced in targeted retinas. Optic nerves from targeted eyes were shown to have reduced macrophage infiltration and improved axonal health. Conclusion Taken together, our results are consistent with Nav1.6 promoting inflammation and contributing to axonal degeneration following demyelination.

Natural killer (NK) cells play critical roles in host defense against infectious agents or neoplastic cells. NK cells provide a rapid innate immune response including the killing of target cells without the need for priming. However, activated NK cells can show improved effector functions. Mast cells are also critical for early host defense against a variety of pathogens and are predominately located at mucosal surfaces and close to blood vessels. Our group has recently shown that virus-infected mast cells selectively recruit NK cells and positively modulate their functions through mechanisms dependent on soluble mediators, such as interferons. Here, we review the possible consequences of this interaction in both host defense and pathologies involving NK cell and mast cell activation.

The postpartum period is an important window during which environmental factors can shape the life-long health of the infant. This time period often coincides with substantial milk consumption either in the form of breast milk or from cow's milk sources, such as infant formulas. Although breast milk is the most beneficial source of nutrients for infants during the first 6 months after birth, its role in regulating food allergy development, through regulation of oral tolerance, is still controversial. Breast milk contains several factors that can impact mucosal immune function, including immune cells, antibodies, microbiota, oligosaccharides, cytokines, and soluble receptors. However, there is considerable variation in the assessed levels of cytokines and soluble receptors between studies and across the lactation period. Most of these cytokines and soluble receptors are absent, or only found in limited quantities, in commercial baby formulas. Differences in content of these pluripotent factors, which impact on both the mother and the neonate, could contribute to the controversy surrounding the role of breast milk regulating oral tolerance. This review highlights current knowledge about the importance of cytokines and soluble receptors in breast milk on the development of oral tolerance and tolerance-relateddisorders. Understanding the mechanisms by which such milk components might promote oral tolerance could aid in the development of improved strategies for allergy prevention.

SummaryBackground Toll-like receptor 2 (TLR2) is a widely expressed pattern recognition receptor critical for innate immunity. TLR2 is also a key regulator of mucosal immunity implicated in the development of allergic disease. TLR2 activators are found in many common foods, but the role of TLR2 in oral tolerance and allergic sensitization to foods is not well understood. Objective The purpose of this study was to evaluate the impacts of TLR2 expression and TLR2 activation on oral tolerance to food antigens in a murine model. Methods Mice were fed ovalbumin (OVA) or peanut butter with or without the addition of low doses of TLR2 activators Pam3CSK4 or FSL-1. Oral tolerance was assessed by analysing antibody responses after a systemic antigen challenge. OVA-specific Tregs were assessed in the Peyer's patches, mesenteric lymph nodes, and spleen in wild-type and TLR2−/− mice. Low-dose Pam3CSK4 was also tested as an oral adjuvant. Results Oral tolerance was successfully induced in both wild-type and TLR2−/− recipient mice, with an associated regulatory T-cell response. Oral TLR2 activation, with low-dose Pam3CSK4 or FSL-1, during oral antigen exposure was found to alter oral tolerance and was associated with the development of substantial IgE and IgA responses to foods upon systemic challenge. Low-dose oral Pam3CSK4 treatment also selectively enhanced antigen-specific IgA responses to oral antigen exposure. Conclusions and Clinical Relevance TLR2 is not necessary for oral tolerance induction, but oral TLR2 activation modulates humoral IgE and IgA responses during tolerance development. Low-dose Pam3CSK4 is also an effective oral adjuvant that selectively enhances IgA production. These observations are pertinent to the optimization of oral allergen immunotherapy and oral vaccine development.

A1 Role of fibrocytes in allergic rhinitis Marie-Ève Côté, Marie-Ève Boulay, Sophie Plante, Jamila Chakir, Louis-Philippe Boulet A2 Patterns of aeroallergens sensitization in Northern Alberta Hanan Ahmed, Maria-Beatriz Ospina, Kyriaki Sideri, Harissios Vliagoftis A3 Addressing acceptable risk for adolescents with Food-Induced Anaphylaxis (FIA) Sara F. Johnson, Roberta L. Woodgate A4 Outcomes of matched related and unrelated bone marrow transplantation after reduced-toxicity conditioning for children suffering from Chronic Granulomatous Disease Guilhem Cros, Pierre Teira, Sonia Cellot, Henrique Bittencourt, Helene Decaluwe, Marie France Vachon, Michel Duval, Elie Haddad A5 Outcomes of patients with severe combined immunodeficiency (SCID) prior to and after initiation of newborn screening for SCID in Ontario Vy H.D. Kim, Anne Pham-Huy, Eyal Grunebaum A6 Detection of regulatory B cells in the airways of subjects with asthma John-Paul Oliveria, Stephanie Phan, Mark W. Tenn, Damian Tworek, Steven G. Smith, Adrian J. Baatjes, Caitlin D. Obminski, Caroline E. Munoz, Tara X. Scime, Roma Sehmi, Gail M Gauvreau A7 Characterization of IgE-expressing B cells in the airways and peripheral blood of allergic asthmatic subjects John-Paul Oliveria, Stephanie Phan, Mark W. Tenn, Brittany M Salter, Steven G Smith, Caitlin D Obminski, Caroline E Munoz, Abbey Schlatman, Tara X Scime, Rick Watson, Roma Sehmi, Gail M Gauvreau A8 Pregnancy: could it be a risk factor for primary immunodeficient patients Roya Sherkat, Razieh Khoshnevisan, Saba Sheikhbahaei A9 Clinical experience with Octagam: a Canadian retrospective chart review Stephen Betschel, Richard Warrington, Robert Schellenberg A10 Kounis syndrome secondary to contrast media with inferior ST elevations and bilateral ischemic stroke Michael N Fein, Jean-Philippe Pelletier A11 Honey bee venom immunotherapy ineffective in bumble bee-induced anaphylaxis: case report and review of literature Manstein Kan, Robert Schellenberg A12 Delayed immune reconstitution occurring after multiple immune complications of hematological stem cell transplantation for a leaky SCID Roxane Labrosse, Guilhem Cros, Pierre Teira, Henrique Bittencourt, Helene Decaluwe, Michel Duval, Elie Haddad A13 Comparison of Three Case Reports of Acquired Angioedema: presentation, management and outcome Raymond Mak, James Loh, Amin Kanani A14 Sitagliptin-associated angioedema not related to concurrent use of ARB or ACE inhibitor Dominik A. Nowak, Paul K. Keith A15 Sneddon-Wilkinson subcorneal pustular dermatosis associated with an IgA monoclonal gammopathy Daniel Pannozzo, Dominik A. Nowak, Hermenio C. Lima A16 Omalizumab can be effective in patients with allergic bronchopulmonary aspergillosis Diana Pham, Hoang Pham, Gonzalo G. Alvarez, Istvan T. Bencze, Krishna B. Sharma, Mark Smith, Shawn Aaron, Jennifer Block, Tara Keays, Judith Leech, David Schneidermen, Jodi Cameron, Jennifer Forgie, Alicia Ring, John W. O’Quinn, Stephanie Santucci, William H. Yang A17 Efficacious use of omalizumab in the treatment of cystic fibrosis Diana Pham, Hoang Pham, Ena Gaudet, Shawn Aaron, Stephanie Santucci, William H. Yang A18 HAE with normal C1-INH with inconsistent response to C1 esterase inhibitor infusion but reliably responsive to icatibant Hoang Pham, Stephanie Santucci, William H. Yang A19 Anaphylaxis reaction to lactase enzyme Mathew R. Voisin, Rozita Borici-Mazi A20 Risk of solid tumor malignancies in patients with primary immune deficiency Kateryna Vostretsova, Donald F. Stark A21 Is it time to adopt the chromogenic assay for measuring C1 esterase inhibitor function in patients with HAE Type 2? Elizabeth Yeboah, Paul K. Keith A22 Emergency department visits for anaphylaxis and allergic reactions Michelle Martin-Rhee, Cheryl Gula, Clare Cheng, Geoff Paltser A23 START: Susceptibility To food Allergies in a Registry of Twins Alizée Dery, Ann Clarke, Kari Nadeau, Laurie Harada, Kimberley Weatherall, Celia Greenwood, Denise Daley, Yuka Asai, Moshe Ben-Shoshan A24 Qualifying the diagnostic approach employed by allergists when managing patients with self-diagnosed non-celiac gluten sensitivity (NCGS) Lee Horgan, Teresa Pun A25 Retrospective analysis on the agreement between skin prick test and serum food specific IgE antibody in adults with suspected food allergy Ling Ling, Maria B. Ospina, Kyriaki Sideri, Harissios Vliagoftis A26 Staple food hypersensitivity from infancy to adolescence: a report from the BAMSE cohort Jennifer L.P. Protudjer, Mirja Vetander, Marianne van Hage, Ola Olén, Magnus Wickman, Anna Bergström A27 Evaluating the impact of supervised epinephrine autoinjector administration during food challenges on perceived parent confidence Timothy Teoh, Christopher Mill, Tiffany Wong, Ingrid Baerg, Angela Alexander, Kyla J. Hildebrand, John Dean, Boris Kuzeljevic, Edmond S. Chan A28 Local immunoglobulin production to Aspergillus fumigatus cystic fibrosis Jonathan Argeny, Mia Gona-Hoepler, Petra Fucik, Edith Nachbaur, Saskia Gruber, Reto Crameri, Andreas Glaser, Zsolt Szépfalusi, Claudio Rhyner, Thomas Eiwegger A29 Extract consumption with skin prick test (SPT) devices Greg. Plunkett, Brad Mire A30 Evaluation of our cases with nonsteroidal anti-inflammatory drug reactions Mehtap Yazicioglu, Ceren Can, Gokce Ciplak A31 Reasons for referral and final diagnoses in a tertiary care pediatric allergy clinic Victoria E. Cook, Kyla J. Hildebrand, Elodie Portales-Casamar, Christopher Mill, Edmond S. Chan A32 Internist referral practices for inpatients with self-reported penicillin allergies at a tertiary care teaching hospital Michael N Fein, Emil P Nashi A33 Assessing the risk of reactions in children with a negative oral challenge after a subsequent use of amoxicillin Sofianne Gabrielli, Christopher Mill, Marie-Noel Primeau, Christine Lejtenyi, Elena Netchiporouk, Alizee Dery, Greg Shand, Moshe Ben-Shoshan A34 Validity of self-reported penicillin allergies Erica Hoe, Joel Liem A35 Effectiveness of allergy-test directed elimination diets in eosinophilic esophagitis Jason K. Ko, David J.T. Huang, Jorge A. Mazza A36 Allergy testing and dietary management in pediatric eosinophilic esophagitis (EoE): A retrospective review of a tertiary Canadian centre’s experience Mary McHenry, Anthony Otley,Wade Watson A37 Visualizing the impact of atopic and allergic skin disease Dominik A. Nowak, John N. Kraft A38 Cystic fibrosis with and without nasal polyposis in pediatric patients: a cross-sectional comparative study Mihaela Paina, Ahmed A. Darwish Hassan, Delia Heroux, Lynn Crawford, Gail Gauvreau, Judah Denburg, Linda Pedder, Paul K. Keith A39 Evaluation of macrolide antibiotic hypersensitivity: the role of oral challenges in children Bahar Torabi, Marie-Noel Primeau, Christine Lejtenyi, Elaine Medoff, Jennifer Mill, Moshe Ben-Shoshan A40 Venom allergy testing: is a graded approach necessary? Jaclyn A. Quirt, Xia Wen, Jonathan Kim, Angel Jimenez Herrero, Harold L. Kim A41 The role of oral challenges in evaluating cephalosporin hypersensitivity reactions in children Magdalena J. Grzyb, Marie-Noël Primeau, Christine Lejtenyi, Elaine Medoff, Jennifer Mill, Moshe Ben-Shoshan A42 Breastfeeding and infant wheeze, atopy and atopic dermatitis: findings from the Canadian Healthy Infant Longitudinal Development Study Meghan B. Azad, Zihang Lu, Allan B. Becker, Padmaja Subbarao, Piushkumar J. Mandhane, Stuart E. Turvey, Malcolm R. Sears, the CHILD Study Investigators A43 IL33 DNA methylation in bronchial epithelial cells is associated to asthma Anne-Marie Boucher-Lafleur, Valérie Gagné-Ouellet, Éric Jacques, Sophie Plante, Jamila Chakir, Catherine Laprise A44 NRF2 mediates the antioxidant response to organic dust-induced oxidative stress in bronchial epithelial cells Michael Chen, Toby McGovern, Mikael Adner, James G. Martin A45 The effects of perinatal distress, immune biomarkers and mother-infant interaction quality on childhood atopic dermatitis (rash) at 18 months Nela Cosic, Henry Ntanda, Gerald Giesbrecht, Anita Kozyrskyj, Nicole Letourneau A46 Examining the immunological mechanisms associated with cow’s milk allergy Bassel Dawod, Jean Marshall A47 Tryptase levels in children presenting with anaphylaxis to the Montréal Children’s Hospital Sarah De Schryver, Michelle Halbrich, Ann Clarke, Sebastian La Vieille, Harley Eisman, Reza Alizadehfar, Lawrence Joseph, Judy Morris, Moshe Ben-Shoshan A48 Secondhand tobacco smoke exposure in infancy and the development of food hypersensitivity from childhood to adolescence Laura Y. Feldman, Jesse D. Thacher, Inger Kull, Erik Melén, Göran Pershagen, Magnus Wickman, Jennifer L. P. Protudjer, Anna Bergström A49 Combined exposure to diesel exhaust and allergen enhances allergic inflammation in the bronchial submucosa of atopic subjects Ali Hosseini, Tillie L. Hackett, Jeremy Hirota, Kelly McNagny, Susan Wilson, Chris Carlsten A50 Comparison of skin-prick test measurements by an automated system against the manual method Saiful Huq, Rishma Chooniedass, Brenda Gerwing, Henry Huang, Diana Lefebvre, Allan Becker A51 The accurate identification and quantification of urinary biomarkers of asthma and COPD through the use of novel DIL- LC-MS/MS methods Mona M. Khamis, Hanan Awad, Kevin Allen, Darryl J. Adamko, Anas El-Aneed A52 Systemic immune pathways associated with the mechanism of Cat-Synthetic Peptide Immuno-Regulatory Epitopes, a novel immunotherapy, in whole blood of cat-allergic people Young Woong Kim, Daniel R. Gliddon, Casey P. Shannon, Amrit Singh, Pascal L. C. Hickey, Anne K. Ellis, Helen Neighbour, Mark Larche, Scott J. Tebbutt A53 Reducing the health disparities: online support for children with asthma and allergies from low-income families Erika Ladouceur, Miriam Stewart, Josh Evans, Jeff Masuda, Nicole Letourneau, Teresa To, Malcolm King A54 Epigenetic association of PSORS1C1 and asthma in the Saguenay-Lac-Saint-Jean asthma study Miriam Larouche, Liming Liang, Catherine Laprise A55 IL-33 induces cytokine and chemokine production in human mast cells Stephanie A. Legere, Ian D. Haidl, Jean-Francois Legaré, Jean S. Marshall A56 Reference ranges for lung clearance index from infancy to adolescence for Canadian population Zihang Lu, Malcolm Sears, Theo J. Moraes, Felix Ratjen, Per Gustafsson, Wendy Lou, Padmaja Subbarao A57 Kingston Allergy Birth Cohort: cohort profile and mother/child characteristics to age 2 Michelle L. North, Elizabeth Lee, Vanessa Omana, Jenny Thiele, Jeff Brook, Anne K. Ellis A58 Cow’s milk protein specific IgE, IgA and IgG4 as a predictor of outcome in oral immunotherapy Tanvir Rahman, Duncan Lejtenyi, Sarah De Schryver, Ryan Fiter, Ciriaco Piccirillo, Moshe Ben-Shoshan, Bruce Mazer A59 Age of peanut introduction and development of reactions and sensitization to peanut Elinor Simons, Allan B. Becker, Rishma Chooniedass, Kyla Hildebrand, Edmond S. Chan, Stuart Turvey, Padmaja Subbarao, Malcolm Sears A60 Multi-omic blood biomarker signatures of the late phase asthmatic response Amrit Singh, Casey P. Shannon, Young Woong Kim, Mari DeMarco, Kim-Anh Le Cao, Gail M. Gauvreau, J. Mark FitzGerald, Louis-Philippe Boulet, Paul M. O’Byrne, Scott J. Tebbutt A61 Early life gut microbial alterations in children diagnosed with asthma by three years of age Leah T. Stiemsma, Marie-Claire Arrieta, Jasmine Cheng, Pedro A. Dimitriu, Lisa Thorson, Sophie Yurist, Boris Kuzeljevic, Diana L. Lefebvre, Padmaja Subbarao, Piush Mandhane, Allan Becker, Malcolm R. Sears, Kelly M. McNagny, Tobias Kollmann, the CHILD Study Investigators, William W. Mohn, B. Brett Finlay, Stuart E. Turvey A62 The relationship between food sensitization and atopic dermatitis at age 1 year in a Canadian birth cohort Maxwell M. Tran, Diana L. Lefebvre, Chinthanie F. Ramasundarahettige, Allan B. Becker, Wei Hao Dai, Padmaja Subbarao, Piush J. Mandhane, Stuart E. Turvey, Malcolm R. Sears A63 Allergen inhalation enhances Toll-like receptor-induced thymic stromal lymphopoietin receptor expression by hematopoietic progenitor cells in mild asthmatics Damian Tworek, Delia Heroux, Seamus N. O’Byrne, Paul M. O’Byrne, Judah A. Denburg A64 The Allergic Rhinitis Clinical Investigator Collaborative – replicated eosinophilia on repeated cumulative allergen challenges in nasal lavage samples Laura Walsh, Mena Soliman, Jenny Thiele, Lisa M. Steacy, Daniel E. Adams, Anne K. Ellis A65 The CHILD Study: optimizing subject retention in pediatric longitudinal cohort research Linda Warner, Mary Ann Mauro, Robby Mamonluk, Stuart E. Turvey A66 Differential expression of C3a and C5a in allergic asthma ChenXi Yang, Amrit Singh, Casey P. Shannon, Young Woong Kim, Ed M. Conway, Scott J. Tebbutt