Group 2 innate lymphoid cells are recruited to the nasal mucosa in patients with aspirin- exacerbated respiratory disease Jacqueline J. Eastman, MD, Kellen.

Slides:

Advertisements

Similar presentations

Nasal challenge with allergen leads to maxillary sinus inflammation

Advertisements

Safety risks for patients with aspirin-exacerbated respiratory disease after acute exposure to selective nonsteroidal anti-inflammatory drugs and COX-2.

Increased numbers of activated group 2 innate lymphoid cells in the airways of patients with severe asthma and persistent airway eosinophilia Steven.

Innate lymphoid cells contribute to allergic airway disease exacerbation by obesity Laetitia Everaere, PhD, Saliha Ait-Yahia, PhD, Olivier Molendi-Coste,

Von Ta, MD, Andrew A. White, MD

Pharmacologic rationale for treating allergic and nonallergic rhinitis

Human group 2 innate lymphoid cells do not express the IL-5 receptor

Katharine M. Woessner, MD, FAAAAI, Andrew A. White, MD, FAAAAI

Reduced TH1/TH17 CD4 T-cell numbers are associated with impaired purified protein derivative–specific cytokine responses in patients with HIV-1 infection

Immunologic defects in 22q11.2 deletion syndrome

Stephen J. Fowler, MD, Gaël Tavernier, PhD, Robert Niven, MD

Anti–IL-5 (mepolizumab) therapy reduces eosinophil activation ex vivo and increases IL- 5 and IL-5 receptor levels Miguel L. Stein, MD, Joyce M. Villanueva,

Type 2 innate lymphoid cells in induced sputum from children with severe asthma Prasad Nagakumar, MBBS, Laura Denney, PhD, Louise Fleming, MD, Andrew.

Safety risks for patients with aspirin-exacerbated respiratory disease after acute exposure to selective nonsteroidal anti-inflammatory drugs and COX-2.

Type 3 innate lymphoid cells induce proliferation of CD94+ natural killer cells Shuo Li, PhD, Hideaki Morita, MD, PhD, Beate Rückert, Sci Tec, Tadech.

Dorothy M. Ryan, MD, Stephen J. Fowler, MD, Robert M. Niven, MD

Katherine N. Cahill, MD, Christina B

Analysis of basophil activation in patients with aspirin-exacerbated respiratory disease Chihiro Mitsui, MD, Keiichi Kajiwara, BSc, Emiko Ono, MD, PhD,

Severe atopic dermatitis is characterized by selective expansion of circulating TH2/TC2 and TH22/TC22, but not TH17/TC17, cells within the skin-homing.

Recurrent anaphylaxis linked to pantoprazole

Natural regulatory T cells in isolated early responders compared with dual responders with allergic asthma Takashi Kinoshita, MD, Adrian Baatjes, MSc,

Profile of eicosanoid generation in aspirin-intolerant asthma and anaphylaxis assessed by new biomarkers Noritaka Higashi, MD, PhD, Haruhisa Mita, PhD,

Reply The Journal of Allergy and Clinical Immunology: In Practice

Blood fibrocytes are recruited during acute exacerbations of chronic obstructive pulmonary disease through a CXCR4-dependent pathway Isabelle Dupin,

Katherine N. Cahill, MD, Jillian C. Bensko, Joshua A

Prominent role of IFN-γ in patients with aspirin-exacerbated respiratory disease John W. Steinke, PhD, Lixia Liu, MD, Phillip Huyett, MD, Julie Negri,

Kathleen R. Bartemes, BA, Gail M. Kephart, BS, Stephanie J

Jerome A. Sigua, MD, Becky Buelow, MD, Dorothy S

Differential expression of functional chemokine receptors on human blood and lung group 2 innate lymphoid cells Cathryn A. Weston, PhD, Batika M.J. Rana,

Increased numbers of activated group 2 innate lymphoid cells in the airways of patients with severe asthma and persistent airway eosinophilia Steven.

Prevalence of aspirin-exacerbated respiratory disease among asthmatic patients: A meta-analysis of the literature Jessica P. Rajan, MD, Nathan E. Wineinger,

Β2 integrins rather than β1 integrins mediate Alternaria-induced group 2 innate lymphoid cell trafficking to the lung Maya R. Karta, PhD, Peter S. Rosenthal,

Specific immunotherapy modifies allergen-specific CD4+ T-cell responses in an epitope- dependent manner Erik Wambre, PhD, Jonathan H. DeLong, BSc, Eddie.

Successful rapid rituximab desensitization in an adolescent patient with nephrotic syndrome: Increase in number of Treg cells after desensitization Metin.

Brent E. Palmer, PhD, Douglas G. Mack, PhD, Allison K

Reply Journal of Allergy and Clinical Immunology

Safety and outcomes of aspirin desensitization for aspirin-exacerbated respiratory disease: A single-center study Jeremy Waldram, MD, Kristen Walters,

Jon Genuneit, MD, MSc Journal of Allergy and Clinical Immunology

Plasma tryptase elevation during aspirin-induced reactions in aspirin-exacerbated respiratory disease Katherine N. Cahill, MD, Katherine Murphy, BA,

Eosinophil production of prostaglandin D2 in patients with aspirin-exacerbated respiratory disease Xin Feng, MD, Madison K. Ramsden, BS, Julie Negri,

MicroRNA-155 is a critical regulator of type 2 innate lymphoid cells and IL-33 signaling in experimental models of allergic airway inflammation Kristina.

Prostaglandin E2 resistance in granulocytes from patients with aspirin-exacerbated respiratory disease Tanya M. Laidlaw, MD, Anya J. Cutler, Molly S.

Basophil counts in PBMC populations during childhood acute wheeze/asthma are associated with future exacerbations Jonatan Leffler, PhD, Anya C. Jones,

Myeloid and plasmacytoid dendritic cells in induced sputum after allergen inhalation in subjects with asthma Benny Dua, MSc, Richard M. Watson, BSc,

Toll-like receptor 2–positive and Toll-like receptor 4–positive cells in adenoids of children exposed to passive smoking Antonio Ricci, MD, M. Antonietta.

Increased frequency of dual-positive TH2/TH17 cells in bronchoalveolar lavage fluid characterizes a population of patients with severe asthma Chaoyu.

Justin R. Chen, MD, Brett L. Buchmiller, MD, David A. Khan, MD

A cluster-randomized trial shows telephone peer coaching for parents reduces children's asthma morbidity Jane M. Garbutt, MB, ChB, Yan Yan, MD, PhD,

What is an “eosinophilic phenotype” of asthma?

Autophagy: Nobel Prize 2016 and allergy and asthma research

Changes in regulatory B-cell levels in bone marrow, blood, and sputum of patients with asthma following inhaled allergen challenge John-Paul Oliveria,

Effect of aging on sputum inflammation and asthma control

Eosinophil production of prostaglandin D2 in patients with aspirin-exacerbated respiratory disease Xin Feng, MD, Madison K. Ramsden, BS, Julie Negri,

Von Ta, MD, Andrew A. White, MD

Anti–IL-5 therapy reduces mast cell and IL-9 cell numbers in pediatric patients with eosinophilic esophagitis Iris M. Otani, MD, Arjun A. Anilkumar,

Hypersensitivity to aspirin: Common eicosanoid alterations in urticaria and asthma Lucyna Mastalerz, MD, PhD, Malgorzta Setkowicz, MD, Marek Sanak, MD,

IL-10, TGF-β, and glucocorticoid prevent the production of type 2 cytokines in human group 2 innate lymphoid cells Noriko Ogasawara, MD, PhD, Julie A.

The Editors' Choice Journal of Allergy and Clinical Immunology

Clinical safety of Food Allergy Herbal Formula-2 (FAHF-2) and inhibitory effect on basophils from patients with food allergy: Extended phase I study

Short course of systemic corticosteroids in sinonasal polyposis: A double-blind, randomized, placebo-controlled trial with evaluation of outcome measures

Nasal challenge with allergen leads to maxillary sinus inflammation

Macrolide antibiotics and asthma treatment

Taylor A. Doherty, MD, Rachel Baum, BS, Robert O

Sublingual immunotherapy for peanut allergy: Clinical and immunologic evidence of desensitization Edwin H. Kim, MD, J. Andrew Bird, MD, Michael Kulis,

Systemic responses after bronchial aspirin challenge in sensitive patients with asthma Joanna S. Makowska, MD, PhD, Janina Grzegorczyk, PhD, Barbara Bienkiewicz,

Alexander S. Kim, MD, Taylor A. Doherty, MD, Maya R

Eosinophil progenitor levels are increased in patients with active pediatric eosinophilic esophagitis David W. Morris, MD, Emily M. Stucke, BA, Lisa.

Invariant natural killer T cells from children with versus without food allergy exhibit differential responsiveness to milk-derived sphingomyelin Soma.

Analysis of basophil activation in patients with aspirin-exacerbated respiratory disease Chihiro Mitsui, MD, Keiichi Kajiwara, BSc, Emiko Ono, MD, PhD,

Early pediatric atopic dermatitis shows only a cutaneous lymphocyte antigen (CLA)+ TH2/TH1 cell imbalance, whereas adults acquire CLA+ TH22/TC22 cell.

Presentation transcript:

Group 2 innate lymphoid cells are recruited to the nasal mucosa in patients with aspirin- exacerbated respiratory disease Jacqueline J. Eastman, MD, Kellen J. Cavagnero, BS, Adam S. Deconde, MD, Alex S. Kim, MD, Maya R. Karta, PhD, David H. Broide, MB, ChB, Bruce L. Zuraw, MD, Andrew A. White, MD, Sandra C. Christiansen, MD, Taylor A. Doherty, MD Journal of Allergy and Clinical Immunology Volume 140, Issue 1, Pages 101-108.e3 (July 2017) DOI: 10.1016/j.jaci.2016.11.023 Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Gating strategy for nasal scrapings and blood ILC2s. The nasal scraping gating strategy was derived from polyp data (see Fig E3). A, Representative nasal sample ILC2 gating from a postdesensitization sample in a patient with AERD. ILC2s were identified as CD45+Lin− lymphocytes that expressed CRTH2. B, Representative parent gating for blood ILC2s. Blood ILC2s were identified as CD45+Lin− lymphocytes that expressed both CD161+ and CRTH2+. C, Representative data of blood CRTH2 plots of baseline, reaction, and postdesensitization samples along with their respective isotypes. FSC, Forward scatter; SSC, side scatter. Journal of Allergy and Clinical Immunology 2017 140, 101-108.e3DOI: (10.1016/j.jaci.2016.11.023) Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 Changes in ILC2 and eosinophil numbers and urinary 11β-PGF2α and LTE4 levels during aspirin desensitization. A, Change in percentage of ILC2s as percentage of all cells in nasal scrapings before challenge, during reaction, and after desensitization was complete (post). Change between baseline and reaction samples was significant (P = .001, paired t test), as well as between reaction and postdesensitization samples (P = .004, paired t test). B, Change in percentage of ILC2s from enriched PBMCs before challenge, during reaction, and after desensitization was complete (post). Change between baseline and reaction samples was significant (P = .031, paired t test). C, Normalized values for nasal scraping and blood ILC2s at the 3 times points. Solid line is for patients with AERD, and dotted lines are for control subjects. D, Eosinophils as percentage of enriched granulocytes. Difference between baseline and reaction samples was significant (P = .044, paired t test). E, Change in levels of the urine PGD2 metabolite 11β-PGF2α. Difference between baseline and reaction samples was significant (P = .008). F, Change in urine LTE4 levels. Difference between baseline and reaction sample was significant (P = .017). ∗P < .05 and ∗∗P < .005. Journal of Allergy and Clinical Immunology 2017 140, 101-108.e3DOI: (10.1016/j.jaci.2016.11.023) Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 Change in ILC2 numbers as related to reaction characteristics. A, Significant correlation was seen between maximum symptom score during reaction and baseline SNOT-22 score (Pearson correlation coefficient, 2-tailed R2 = 0.490, P = .036). B, Significant correlation was seen between maximum symptom score and fold increase in nasal scraping ILC2 numbers during the reaction (Pearson correlation coefficient, R2 = 0.472, P = .028). C, Correlation between ILC2 numbers in the blood and time for reaction to subside (Pearson correlation coefficient, 2-tailed R2 = 0.395, P = .038). Journal of Allergy and Clinical Immunology 2017 140, 101-108.e3DOI: (10.1016/j.jaci.2016.11.023) Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig E1 Modified AERD symptom score. Journal of Allergy and Clinical Immunology 2017 140, 101-108.e3DOI: (10.1016/j.jaci.2016.11.023) Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig E2 NSAID challenge and desensitization protocols. UCSD, University of California, San Diego. Journal of Allergy and Clinical Immunology 2017 140, 101-108.e3DOI: (10.1016/j.jaci.2016.11.023) Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig E3 Gating strategy for nasal scrapings and blood ILC2s derived from nasal polyps. Representative gating from a surgically removed nasal polyp from a patient who subsequently underwent aspirin desensitization. Nasal polyp ILC2s were identified as CD45+ lymphocytes that are Lin− and express either CRTH2 (A) or GATA-3 (B). FSC, Forward scatter; SSC, side scatter. Journal of Allergy and Clinical Immunology 2017 140, 101-108.e3DOI: (10.1016/j.jaci.2016.11.023) Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions