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  1. Article ; Online: Dietary and Microbial Determinants in Food Allergy.

    Stephen-Victor, Emmanuel / Crestani, Elena / Chatila, Talal A

    Immunity

    2020  Volume 53, Issue 2, Page(s) 277–289

    Abstract: The steep rise in food allergy (FA) has evoked environmental factors involved in disease pathogenesis, including the gut microbiota, diet, and their metabolites. Early introduction of solid foods synchronizes with the "weaning reaction," a time during ... ...

    Abstract The steep rise in food allergy (FA) has evoked environmental factors involved in disease pathogenesis, including the gut microbiota, diet, and their metabolites. Early introduction of solid foods synchronizes with the "weaning reaction," a time during which the microbiota imprints durable oral tolerance. Recent work has shown that children with FA manifest an early onset dysbiosis with the loss of Clostridiales species, which promotes the differentiation of ROR-γt
    MeSH term(s) Animals ; Clostridiales/isolation & purification ; Desensitization, Immunologic/methods ; Diet ; Dysbiosis/microbiology ; Food Hypersensitivity/immunology ; Gastrointestinal Microbiome/physiology ; Humans ; Immune Tolerance/immunology ; Immunoglobulin E/immunology ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Nuclear Receptor Subfamily 1, Group F, Member 3 ; RORC protein, human ; Immunoglobulin E (37341-29-0)
    Language English
    Publishing date 2020-08-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2020.07.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Piloting a multidisciplinary group education session to support caregivers of children with food protein-induced enterocolitis syndrome (FPIES).

    LeBovidge, Jennifer / Elverson, Wendy / Esty, Brittany / Maciag, Michelle C / Syverson, Erin Phillips / Grossman, Mia / Crestani, Elena / Queheillalt, Dianna / Okazaki, Yoshiko / Perez, Olga / Hait, Elizabeth J / Bartnikas, Lisa M

    The journal of allergy and clinical immunology. In practice

    2023  Volume 11, Issue 10, Page(s) 3260–3262.e1

    Language English
    Publishing date 2023-07-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2843237-X
    ISSN 2213-2201 ; 2213-2198
    ISSN (online) 2213-2201
    ISSN 2213-2198
    DOI 10.1016/j.jaip.2023.06.053
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  3. Article ; Online: A common IL-4 receptor variant promotes asthma severity via a T

    Benamar, Mehdi / Harb, Hani / Chen, Qian / Wang, Muyun / Chan, Tsz Man Fion / Fong, Jason / Phipatanakul, Wanda / Cunningham, Amparito / Ertem, Deniz / Petty, Carter R / Mousavi, Amirhosein J / Sioutas, Constantinos / Crestani, Elena / Chatila, Talal A

    Allergy

    2022  Volume 77, Issue 11, Page(s) 3377–3387

    Abstract: Background: The mechanisms by which genetic and environmental factors interact to promote asthma remain unclear. Both the IL-4 receptor alpha chain R576 (IL-4RαR576) variant and Notch4 license asthmatic lung inflammation by allergens and ambient ... ...

    Abstract Background: The mechanisms by which genetic and environmental factors interact to promote asthma remain unclear. Both the IL-4 receptor alpha chain R576 (IL-4RαR576) variant and Notch4 license asthmatic lung inflammation by allergens and ambient pollutant particles by subverting lung regulatory T (T
    Objective: We examined the interaction between IL-4RαR576 and Notch4 in promoting asthmatic inflammation.
    Methods: Peripheral blood mononuclear cells (PBMCs) of asthmatics were analyzed for T helper type 2 cytokine production and Notch4 expression on T
    Results: Asthmatics carrying the IL4R
    Conclusion: These results identify an IL-4RαR576-regulated GRB2-IL-6-Notch4 circuit that promotes asthma severity by subverting lung T
    MeSH term(s) Animals ; Mice ; Asthma/genetics ; Disease Models, Animal ; Inflammation ; Interleukin-6/metabolism ; Leukocytes, Mononuclear/metabolism ; Lung ; Mice, Inbred BALB C ; Pneumonia/metabolism ; Receptors, Interleukin-4/metabolism ; T-Lymphocytes, Regulatory
    Chemical Substances Interleukin-6 ; Receptors, Interleukin-4 ; Grb2 protein, mouse
    Language English
    Publishing date 2022-07-25
    Publishing country Denmark
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 391933-x
    ISSN 1398-9995 ; 0105-4538
    ISSN (online) 1398-9995
    ISSN 0105-4538
    DOI 10.1111/all.15444
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Atopic Dermatitis Mediates the Association Between an IL4RA Variant and Food Allergy in School-Aged Children.

    Banzon, Tina M / Kelly, Michael S / Bartnikas, Lisa M / Sheehan, William J / Cunningham, Amparito / Harb, Hani / Crestani, Elena / Valeri, Linda / Greco, Kimberly F / Chatila, Talal A / Phipatanakul, Wanda / Lai, Peggy S

    The journal of allergy and clinical immunology. In practice

    2022  Volume 10, Issue 8, Page(s) 2117–2124.e4

    Abstract: Background: Atopic dermatitis (AD) and food allergy (FA) may share genetic risk factors. It is unknown whether genetic factors directly cause FA or are mediated through AD, as the dual-allergen hypothesis suggests.: Objective: To test the hypothesis ... ...

    Abstract Background: Atopic dermatitis (AD) and food allergy (FA) may share genetic risk factors. It is unknown whether genetic factors directly cause FA or are mediated through AD, as the dual-allergen hypothesis suggests.
    Objective: To test the hypothesis that AD mediates the relationship between an IL-4 receptor alpha chain gene (IL4RA) variant, the human IL-4 receptor alpha chain protein-R576 polymorphism, and FA.
    Methods: A total of 433 children with asthma enrolled in the School Inner-City Asthma Study underwent genotyping for the IL4RA
    Results: AD was reported in 193 (45%) and FA in 80 children (19%). Each risk allele increased odds of AD 1.39-fold ([1.03-1.87], P = .03), and AD increased odds of FA 3.67-fold ([2.05- 6.57], P < .01). There was an indirect effect of genotype, mediated by AD, predicting FA; each risk allele increased the odds of FA by 1.13 (odds ratio [95% CI], Q/R = 1.13 [1.02-1.24], R/R = 1.28 [1.04-1.51]; P < .01). Each risk allele increased the odds of severe FA symptoms 2.68-fold ([1.26-5.71], P = .01).
    Conclusions: In a cohort of children with asthma, AD is part of the causal pathway between an IL4RA variant and FA. This variant is associated with increased risk of severe FA reactions. Addressing AD in children with an IL4RA polymorphism may modulate the risk of FA.
    MeSH term(s) Allergens ; Asthma/complications ; Asthma/epidemiology ; Asthma/genetics ; Child ; Dermatitis, Atopic/complications ; Dermatitis, Atopic/epidemiology ; Dermatitis, Atopic/genetics ; Food Hypersensitivity/complications ; Food Hypersensitivity/epidemiology ; Food Hypersensitivity/genetics ; Genotype ; Humans ; Interleukin-4 Receptor alpha Subunit/genetics
    Chemical Substances Allergens ; IL4R protein, human ; Interleukin-4 Receptor alpha Subunit
    Language English
    Publishing date 2022-05-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2843237-X
    ISSN 2213-2201 ; 2213-2198
    ISSN (online) 2213-2201
    ISSN 2213-2198
    DOI 10.1016/j.jaip.2022.04.042
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Autoantibodies are associated with disease progression in idiopathic pulmonary fibrosis.

    Koether, Katerina / Besnard, Valérie / Sandig, Hilary / Carruthers, Alan / Miranda, Elena / Grootenboer-Mignot, Sabine / Taillé, Camille / Chevret, Sylvie / Valeyre, Dominique / Nunes, Hilario / Israel-Biet, Dominique / Lim, Wei Keat / Cottin, Vincent / Corkill, Dominic / Dobson, Claire / Groves, Maria / Ferraro, Franco / Guenzi, Edouard / Huang, Ling /
    Sulikowski, Michal / Mailleux, Arnaud / Murray, Lynne Anne / Mustelin, Thomas / Strickland, Ian / Sleeman, Matthew A / Crestani, Bruno

    The European respiratory journal

    2023  Volume 61, Issue 5

    Abstract: Several reports have highlighted a potential role of autoreactive B-cells and autoantibodies that correlates with increased disease severity in patients with idiopathic pulmonary fibrosis (IPF). Here we show that patients with IPF have an altered B-cell ... ...

    Abstract Several reports have highlighted a potential role of autoreactive B-cells and autoantibodies that correlates with increased disease severity in patients with idiopathic pulmonary fibrosis (IPF). Here we show that patients with IPF have an altered B-cell phenotype and that those subjects who have autoantibodies against the intermediate filament protein periplakin (PPL) have a significantly worse outcome in terms of progression-free survival. Using a mouse model of lung fibrosis, we demonstrate that introducing antibodies targeting the endogenous protein PPL (mimicking naturally occurring autoantibodies seen in patients) directly in the lung increases lung injury, inflammation, collagen and fibronectin expression through direct activation of follicular dendritic cells, which in turn activates and drives proliferation of fibroblasts. This fibrocyte population was also observed in fibrotic foci of patients with IPF and was increased in peripheral blood of IPF patients compared to aged-matched controls. This study reiterates the complex and heterogeneous nature of IPF, identifying new pathways that may prove suitable for therapeutic intervention.
    MeSH term(s) Humans ; Autoantibodies ; Idiopathic Pulmonary Fibrosis/drug therapy ; Lung/metabolism ; Disease Progression ; Fibroblasts/metabolism
    Chemical Substances Autoantibodies
    Language English
    Publishing date 2023-05-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.02381-2021
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  6. Article ; Online: SARS-CoV-2-specific T cell responses in patients with multisystem inflammatory syndrome in children.

    Lam, Ki Pui / Chiñas, Marcos / Julé, Amélie M / Taylor, Maria / Ohashi, Marina / Benamar, Mehdi / Crestani, Elena / Son, Mary Beth F / Chou, Janet / Gebhart, Catherine / Chatila, Talal / Newburger, Jane / Randolph, Adrienne / Gutierrez-Arcelus, Maria / Henderson, Lauren A

    Clinical immunology (Orlando, Fla.)

    2022  Volume 243, Page(s) 109106

    Abstract: Multisystem inflammatory syndrome in children (MIS-C) is a severe complication of SARS-CoV-2 infections that occurs in the pediatric population. We sought to characterize T cell responses in MIS-C compared to COVID-19 and pediatric hyperinflammatory ... ...

    Abstract Multisystem inflammatory syndrome in children (MIS-C) is a severe complication of SARS-CoV-2 infections that occurs in the pediatric population. We sought to characterize T cell responses in MIS-C compared to COVID-19 and pediatric hyperinflammatory syndromes. MIS-C was distinct from COVID-19 and hyperinflammatory syndromes due to an expansion of T cells expressing TRBV11-2 that was not associated with HLA genotype. Children diagnosed with MIS-C, but who were negative for SARS-CoV-2 by PCR and serology, did not display Vβ skewing. There was no difference in the proportion of T cells that became activated after stimulation with SARS-CoV-2 peptides in children with MIS-C compared to convalescent COVID-19. The frequency of SARS-CoV-2-specific TCRs and the antigens recognized by these TCRs were comparable in MIS-C and COVID-19. Expansion of Vβ11-2
    MeSH term(s) COVID-19/complications ; Child ; Connective Tissue Diseases ; Humans ; SARS-CoV-2 ; Systemic Inflammatory Response Syndrome ; T-Lymphocytes
    Language English
    Publishing date 2022-08-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2022.109106
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  7. Article ; Online: Author Correction: A regulatory T cell Notch4-GDF15 axis licenses tissue inflammation in asthma.

    Harb, Hani / Stephen-Victor, Emmanuel / Crestani, Elena / Benamar, Mehdi / Massoud, Amir / Cui, Ye / Charbonnier, Louis-Marie / Arbag, Sena / Baris, Safa / Cunnigham, Amparito / Leyva-Castillo, Juan Manuel / Geha, Raif S / Mousavi, Amirhosein J / Guennewig, Boris / Schmitz-Abe, Klaus / Sioutas, Constantinos / Phipatanakul, Wanda / Chatila, Talal A

    Nature immunology

    2021  Volume 22, Issue 6, Page(s) 794–795

    Abstract: A Correction to this paper has been published: https://doi.org/10.1038/s41590-021-00929-x. ...

    Abstract A Correction to this paper has been published: https://doi.org/10.1038/s41590-021-00929-x.
    Language English
    Publishing date 2021-05-25
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-021-00929-x
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  8. Article: Dietary Mannan Oligosaccharides Modulate Gut Inflammatory Response and Improve Duodenal Villi Height in Post-Weaning Piglets Improving Feed Efficiency.

    Agazzi, Alessandro / Perricone, Vera / Omodei Zorini, Fabio / Sandrini, Silvia / Mariani, Elena / Jiang, Xian-Ren / Ferrari, Alessandra / Crestani, Maurizio / Nguyen, Thi Xuan / Bontempo, Valentino / Domeneghini, Cinzia / Savoini, Giovanni

    Animals : an open access journal from MDPI

    2020  Volume 10, Issue 8

    Abstract: The aim of this study was to evaluate the effects of mannan oligosaccharides (MOS) on gut health and performance in post-weaning piglets. In total, 40 piglets were divided into two experimental groups and fed a basal diet with (TRT) or without (CON) 0.2% ...

    Abstract The aim of this study was to evaluate the effects of mannan oligosaccharides (MOS) on gut health and performance in post-weaning piglets. In total, 40 piglets were divided into two experimental groups and fed a basal diet with (TRT) or without (CON) 0.2% mannan oligosaccharides for 35 days. Growth performance was determined weekly and faecal microbial composition on days 0, 14 and 35. On day 36, histometrical evaluations were performed on duodenal, jejunal, ileal, and colon samples. mRNA gene expression of inflammation-related genes was evaluated in samples of ileal Peyer's patches (IPP). MOS administration improved feed efficiency in the last two weeks of the trial (
    Language English
    Publishing date 2020-07-28
    Publishing country Switzerland
    Document type Journal Article
    ISSN 2076-2615
    ISSN 2076-2615
    DOI 10.3390/ani10081283
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  9. Article ; Online: A common IL‐4 receptor variant promotes asthma severity via a Treg cell GRB2‐IL‐6‐Notch4 circuit

    Benamar, Mehdi / Harb, Hani / Chen, Qian / Wang, Muyun / Chan, Tsz Man Fion / Fong, Jason / Phipatanakul, Wanda / Cunningham, Amparito / Ertem, Deniz / Petty, Carter R. / Mousavi, Amirhosein J. / Sioutas, Constantinos / Crestani, Elena / Chatila, Talal A.

    Allergy. 2022 Nov., v. 77, no. 11, p. 3377-3387

    2022  , Page(s) 3377–3387

    Abstract: BACKGROUND: The mechanisms by which genetic and environmental factors interact to promote asthma remain unclear. Both the IL‐4 receptor alpha chain R576 (IL‐4RαR576) variant and Notch4 license asthmatic lung inflammation by allergens and ambient ... ...

    Abstract BACKGROUND: The mechanisms by which genetic and environmental factors interact to promote asthma remain unclear. Both the IL‐4 receptor alpha chain R576 (IL‐4RαR576) variant and Notch4 license asthmatic lung inflammation by allergens and ambient pollutant particles by subverting lung regulatory T (Tᵣₑg) cells in an IL‐6‐dependent manner. OBJECTIVE: We examined the interaction between IL‐4RαR576 and Notch4 in promoting asthmatic inflammation. METHODS: Peripheral blood mononuclear cells (PBMCs) of asthmatics were analyzed for T helper type 2 cytokine production and Notch4 expression on Tᵣₑg cells as a function of IL4Rᴿ⁵⁷⁶ allele. The capacity of IL‐4RαR576 to upregulate Notch4 expression on Tᵣₑg cells to promote severe allergic airway inflammation was further analyzed in genetic mouse models. RESULTS: Asthmatics carrying the IL4Rᴿ⁵⁷⁶ allele had increased Notch4 expression on their circulating Tᵣₑg cells as a function of disease severity and serum IL‐6. Mice harboring the Il4raᴿ⁵⁷⁶ allele exhibited increased Notch4‐dependent allergic airway inflammation that was inhibited upon Tᵣₑg cell‐specific Notch4 deletion or treatment with an anti‐Notch4 antibody. Signaling via IL‐4RαR576 upregulated the expression in lung Tᵣₑg cells of Notch4 and its downstream mediators Yap1 and beta‐catenin, leading to exacerbated lung inflammation. This upregulation was dependent on growth factor receptor‐bound protein 2 (GRB2) and IL‐6 receptor. CONCLUSION: These results identify an IL‐4RαR576‐regulated GRB2‐IL‐6‐Notch4 circuit that promotes asthma severity by subverting lung Tᵣₑg cell function.
    Keywords CD4-positive T-lymphocytes ; alleles ; antibodies ; asthma ; beta catenin ; blood serum ; disease severity ; inflammation ; interleukin-4 ; interleukin-6 ; lungs ; mice ; pollutants
    Language English
    Dates of publication 2022-11
    Size p. 3377-3387
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    Note JOURNAL ARTICLE
    ZDB-ID 391933-x
    ISSN 1398-9995 ; 0105-4538
    ISSN (online) 1398-9995
    ISSN 0105-4538
    DOI 10.1111/all.15444
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  10. Article ; Online: Author Correction: A regulatory T cell Notch4-GDF15 axis licenses tissue inflammation in asthma.

    Harb, Hani / Stephen-Victor, Emmanuel / Crestani, Elena / Benamar, Mehdi / Massoud, Amir / Cui, Ye / Charbonnier, Louis-Marie / Arbag, Sena / Baris, Safa / Cunnigham, Amparito / Leyva-Castillo, Juan Manuel / Geha, Raif S / Mousavi, Amirhosein J / Guennewig, Boris / Schmitz-Abe, Klaus / Sioutas, Constantinos / Phipatanakul, Wanda / Chatila, Talal A

    Nature immunology

    2020  Volume 22, Issue 1, Page(s) 100

    Language English
    Publishing date 2020-11-19
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-020-00841-w
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