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Articoli di riviste sul tema "IgE"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

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1

Mastrangelo, G., C. Veller Fornasa, S. Pavanello, et al. "Polyaromatic Hydrocarbons Administered in Humans by Dermal Route Increase Total IgE." International Journal of Immunopathology and Pharmacology 16, no. 2 (2003): 145–50. http://dx.doi.org/10.1177/039463200301600208.

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Inhalation of polyaromatic hydrocarbons (PAHs) extracted from diesel exhaust particles (DEP) enhances local (nasal) production of IgE in humans. The aim of the present research is to investigate whether in humans dermal exposure to PAHs which are not extracted from DEPs increases serum IgE and whether host factors modify the immunologic effect. In thirty-two patients with acute psoriatic lesions, a cream containing 3% of coal tar (which holds a variety of PAHs) was applied to the skin for 24 hours. Serum IgE were measured before (IgE0) and four (IgE4) and eight (IgE8) days after application. R

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2

Ledford, Dennis K. "Increased IgE in IgA Deficiency." Journal of Allergy and Clinical Immunology: In Practice 5, no. 6 (2017): 1795. http://dx.doi.org/10.1016/j.jaip.2017.07.013.

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3

Corrado, Alessia, Richard P. Ramonell, Matthew C. Woodruff, et al. "Extrafollicular IgD+ B cells generate IgE antibody secreting cells in the nasal mucosa." Mucosal Immunology 14, no. 5 (2021): 1144–59. http://dx.doi.org/10.1038/s41385-021-00410-w.

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AbstractIncreased IgE is a typical feature of allergic rhinitis. Local class-switch recombination has been intimated but B cell precursors and mechanisms remain elusive. Here we describe the dynamics underlying the generation of IgE-antibody secreting cells (ASC) in human nasal polyps (NP), mucosal tissues rich in ASC without germinal centers (GC). Using VH next generation sequencing, we identified an extrafollicular (EF) mucosal IgD+ naïve-like intermediate B cell population with high connectivity to the mucosal IgE ASC. Mucosal IgD+ B cells, express germline epsilon transcripts and predomina

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4

Kolopp-Sarda, M. N., and G. C. Faure. "Pourquoi les immunoglobulines s’appellent-elles IgG, IgA, IgM, IgD et IgE ?" Revue Francophone des Laboratoires 2016, no. 484 (2016): 57–58. http://dx.doi.org/10.1016/s1773-035x(16)30250-7.

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5

Abbal, Michel. "IgE totales et IgE spécifiques." Bio Tribune Magazine 6, no. 1 (2003): 20–22. http://dx.doi.org/10.1007/bf03010285.

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6

Nawata, Y., T. Koike, H. Hosokawa, H. Tomioka, and S. Yoshida. "Anti-IgE autoantibody in patients with atopic dermatitis." Journal of Immunology 135, no. 1 (1985): 478–82. http://dx.doi.org/10.4049/jimmunol.135.1.478.

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Abstract (sommario):

Abstract The anti-IgE autoantibody in the IgG class was detected in 39/45 (86.7%) patients with atopic dermatitis by using a newly established solid-phase enzyme immunoassay. The epsilon-chain specificity of the anti-IgE autoantibody was confirmed by competitive inhibition by using human IgG, IgA, IgM, IgD, IgE, and heat-denatured IgE protein. Significant correlations were observed between the levels of the anti-IgE autoantibody and the serum IgE. Gel filtration studies indicated that the anti-IgE autoantibody in sera from atopic dermatitis was mainly present in the form of an immune complex w

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7

Sabra, Aderbal, Joseph A. Bellanti, Jonathan M. Rais, Henry J. Castro, Julia Mendez de Inocencio, and Selma Sabra. "IgE and non-IgE food allergy." Annals of Allergy, Asthma & Immunology 90, no. 6 (2003): 71–76. http://dx.doi.org/10.1016/s1081-1206(10)61664-x.

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8

Boltansky, Howard, Jean Dyer, Steve Esworthy, and Michael Kaliner. "IgE-immunotoxins. I. IgE-intact ricin." Immunopharmacology 14, no. 1 (1987): 35–45. http://dx.doi.org/10.1016/0162-3109(87)90007-5.

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9

Xie, Liping, John T. Schroeder, Jacqueline M. Langdon, Rebecca S. Sora-Scott, Toshiaki Kawakami, and Susan M. MacDonald. "Human IgE+ and IgE− are not equivalent to mouse highly cytokinergic IgE." Journal of Allergy and Clinical Immunology 121, no. 4 (2008): 1027–33. http://dx.doi.org/10.1016/j.jaci.2007.12.1157.

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10

DECLERCK, L., M. WESTEDT, A. CATS, et al. "391 IgE, IgE-containing circulating immune complexes (IgE-CIC) IgE-rheumatoid factor (RF) and skin IgE-deposition in rheumatoid arthritis (RA) patients (pts)." Journal of Allergy and Clinical Immunology 75, no. 1 (1985): 202. http://dx.doi.org/10.1016/0091-6749(85)90527-5.

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11

Pankovics, Gergő. "Az ige jelentésének összefüggése az igei vonzatstruktúrával." Magyar Nyelvőr 145, no. 2 (2021): 211–19. http://dx.doi.org/10.38143/nyr.2021.2.211.

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12

Adachi, M., N. Noro, T. Nagai, and J. Yodoi. "Regulatory mechanism of IgA and IgE production." Annales de l'Institut Pasteur / Immunologie 136, no. 3 (1985): 403–6. http://dx.doi.org/10.1016/s0769-2625(85)80014-3.

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13

Arnautou, Pierre, Carine Garcia-Hejl, C. Hubert, and P. Vest. "Les myélomes multiples à IgD et IgE." Revue de biologie médicale 347, no. 2 (2019): 5–15. https://doi.org/10.3917/rbm.347.0005.

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Abstract (sommario):

Les myélomes multiples à IgD et IgE sont des hémopathies rares, représentant respectivement 2 % et 0,1 % de l’ensemble des myélomes multiples. Depuis leurs premières descriptions dans les années 60, un nombre limité de cas a été rapporté dans la littérature. Leurs aspects cliniques semblent proches des autres catégories de myélome multiple. Cependant, ces pathologies semblent plus agressives et associées à une moins bonne survie. Compte tenu de la rareté des IgE monoclonales, il n’est pas possible de mettre en évidence des caractéristiques cliniques et biologiques communes. En revanche, pour l

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14

Marinkovich, Vincent A., and Neil Woodmansey. "Total IgE and Allergen-Specific IgE Assays." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 25, no. 2 (1988): 195–96. http://dx.doi.org/10.1177/000456328802500214.

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15

Boltansky, Howard, Jay Slater, Richard Youle, Chaviva Isersky, and Michael Kaliner. "IgE-immunotoxins. II. IgE-ricin A-chain." Immunopharmacology 14, no. 1 (1987): 47–62. http://dx.doi.org/10.1016/0162-3109(87)90008-7.

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16

Vassella, Claudia C., Alain L. de Weck, and Beda M. Stadler. "Influence of IgE Fragments on IgE Determination." International Archives of Allergy and Immunology 92, no. 3 (1990): 272–80. http://dx.doi.org/10.1159/000235189.

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17

Besu, Irina, Tatjana Srdic-Rajic, Ivana Matic, et al. "The absence of immunoreactivity to donkey's milk in patients with recurrent aphthous ulcers and immunoreactivity to cow's milk." Food and Agricultural Immunology 28, no. 3 (2017): 452–62. https://doi.org/10.1080/09540105.2017.1293017.

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Abstract (sommario):

Despite the numerous benefits of milk constituents for human health, a considerable number of the general population follow a milk-restricted diet due to clinically confirmed or self-assessed adverse reactions to cow’s milk consumption. Recurrent aphthous ulcers (RAU) are currently one of the most common oral disorders, with a worldwide distribution and insufficiently defined etiology, which, among other factors, implies the immunological reaction to food proteins. The aim of this study was to determine the immune-reactivity to donkey’s milk proteins in patients with RAU and compar

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18

Harfi, Harb A., and John T. Godwin. "Normal Serum Levels of IgG, IgA, IgM, IgD, and IgE in Saudi Arabia." Annals of Saudi Medicine 5, no. 2 (1985): 99–104. http://dx.doi.org/10.5144/0256-4947.1985.99.

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19

Salonen, Eeva-Marjatta, Tapani Hovi, Olli Meurman, Timo Vesikari, and Antti Vaheri. "Kinetics of specific IgA, IgD, IgE, IgG, and IgM antibody responses in rubella." Journal of Medical Virology 16, no. 1 (1985): 1–9. http://dx.doi.org/10.1002/jmv.1890160102.

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20

Nakajima, T., M. Sarfati, and G. Delespesse. "Relationship between human IgE-binding factors (IgE-BF) and lymphocyte receptors for IgE." Journal of Immunology 139, no. 3 (1987): 848–54. http://dx.doi.org/10.4049/jimmunol.139.3.848.

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Abstract This study indicates that human IgE-binding factors (IgE-BF) found in the cellfree culture supernatant (CSN) of Fc epsilon R-bearing B cells are breakdown products of the surface Fc epsilon R. This conclusion is suggested by the following observations. 1) Fc epsilon R and IgE-BF share several antigenic determinants as shown by immunoprecipitation with several Mab to Fc epsilon R (MabER) and SDS-PAGE analysis of the precipitates. 2) Upon incubation at 37 degrees C, normal tonsillar lymphocytes lose their Fc epsilon R and this is associated in a time-related manner with the release in t

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21

Novak, Natalija, Stefan Kraft, and Thomas Bieber. "IgE receptors." Current Opinion in Immunology 13, no. 6 (2001): 721–26. http://dx.doi.org/10.1016/s0952-7915(01)00285-0.

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22

Josephs, Debra H., James F. Spicer, Panagiotis Karagiannis, Hannah J. Gould, and Sophia N. Karagiannis. "IgE immunotherapy." mAbs 6, no. 1 (2013): 54–72. http://dx.doi.org/10.4161/mabs.27029.

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23

Hegewisch, S., K. Mainzer, and D. Braumann. "IgE myelomatosis." Blut 55, no. 1 (1987): 55–60. http://dx.doi.org/10.1007/bf00319644.

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24

Delespesse, G., M. Sarfati, and C. Heusser. "IgE synthesis." Current Opinion in Immunology 2, no. 4 (1990): 506–12. http://dx.doi.org/10.1016/0952-7915(90)90003-y.

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25

ROBBANA-BARNAT, SAIDA, and JACQUES FRADIN. "Cereal Grains: IgE- and Non-IgE-mediated Reactions." Journal of Nutritional & Environmental Medicine 7, no. 1 (1997): 35–46. http://dx.doi.org/10.1080/13590849762781.

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26

Zopf, Yurdagül, and Walburga Dieterich. "IgE- und nicht IgE-vermittelte Nahrungsmittelallergien – ein Überblick." DMW - Deutsche Medizinische Wochenschrift 149, no. 18 (2024): 1080–88. http://dx.doi.org/10.1055/a-2194-9047.

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27

Bloch-Michel, E., S. Liotet, M. P. Lecorvec, and P. M. Cerqueti. "IgE des larmes, IgE sériques et tests cutanés." Revue Française d'Allergologie et d'Immunologie Clinique 25, no. 3 (1985): 135–39. http://dx.doi.org/10.1016/s0335-7457(85)80014-9.

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28

de Macario, Everly Conway, A. J. L. Macario, and R. J. Jovell. "Slide immunoenzymatic assay for human IgE (SIA-IgE)." Journal of Immunological Methods 90, no. 1 (1986): 137–41. http://dx.doi.org/10.1016/0022-1759(86)90394-7.

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29

Platzer, Barbara, Floortje Ruiter, John van der Mee, and Edda Fiebiger. "Soluble IgE receptors—Elements of the IgE network." Immunology Letters 141, no. 1 (2011): 36–44. http://dx.doi.org/10.1016/j.imlet.2011.08.004.

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30

Haniuda, Kei, Saori Fukao, Tadahiro Kodama, Hitoshi Hasegawa, and Daisuke Kitamura. "Autonomous membrane IgE signaling prevents IgE-memory formation." Nature Immunology 17, no. 9 (2016): 1109–17. http://dx.doi.org/10.1038/ni.3508.

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31

DOAN, S. "IgE, anti-IgE, and allergic keratoconjunctivitis - part 1." Acta Ophthalmologica 92 (August 20, 2014): 0. http://dx.doi.org/10.1111/j.1755-3768.2014.3271.x.

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32

CHIAMBARETTA, F. "IgE, anti-IgE, and allergic keratoconjunctivitis - part 2." Acta Ophthalmologica 92 (August 20, 2014): 0. http://dx.doi.org/10.1111/j.1755-3768.2014.3272.x.

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33

Delespesse, G., and M. Sarfati. "IgE-binding factors (soluble CD23) and IgE regulation." Research in Immunology 141, no. 1 (1990): 75–77. http://dx.doi.org/10.1016/0923-2494(90)90105-8.

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34

Zopf, Yurdagül, and Walburga Dieterich. "IgE- und nicht IgE-vermittelte Nahrungsmittelallergien – ein Überblick." Gastroenterologie up2date 21, no. 01 (2025): 77–89. https://doi.org/10.1055/a-2504-3582.

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35

Ando, Tomoaki, and Jiro Kitaura. "Tuning IgE: IgE-Associating Molecules and Their Effects on IgE-Dependent Mast Cell Reactions." Cells 10, no. 7 (2021): 1697. http://dx.doi.org/10.3390/cells10071697.

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Abstract (sommario):

The recent emergence of anti-immunoglobulin E (IgE) drugs and their candidates for humans has endorsed the significance of IgE-dependent pathways in allergic disorders. IgE is distributed locally in the tissues or systemically to confer a sensory mechanism in a domain of adaptive immunity to the otherwise innate type of effector cells, namely, mast cells and basophils. Bound on the high-affinity IgE receptor FcεRI, IgE enables fast memory responses against revisiting threats of venoms, parasites, and bacteria. However, the dysregulation of IgE-dependent reactions leads to potentially life-thre

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36

Haba, S., and A. Nisonoff. "Inhibition of IgE synthesis by anti-IgE: role in long-term inhibition of IgE synthesis by neonatally administered soluble IgE." Proceedings of the National Academy of Sciences 87, no. 9 (1990): 3363–67. http://dx.doi.org/10.1073/pnas.87.9.3363.

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37

Ezeamuzie, Charles I., Raja'a Al-Attiyah, Puthiyaveetil K. Shihab та Reem Al-Radwan. "Low-affinity IgE receptor (FcεRII)-mediated activation of human monocytes by both monomeric IgE and IgE/anti-IgE immune complex". International Immunopharmacology 9, № 9 (2009): 1110–14. http://dx.doi.org/10.1016/j.intimp.2009.05.009.

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38

Zhang, X. H., C. Werner-Favre, H. Y. Tang, N. Brouwers, J. Y. Bonnefoy, and R. H. Zubler. "IL-4-dependent IgE switch in membrane IgA-positive human B cells." Journal of Immunology 147, no. 9 (1991): 3001–4. http://dx.doi.org/10.4049/jimmunol.147.9.3001.

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Abstract (sommario):

Abstract IgE responses by human B cells, separated according to membrane Ig classes, were analyzed in a clonal assay using EL-4 thymoma cells as helper cells, T cell supernatant, and rIL-4. In cultures seeded by means of the autoclone apparatus of the FACS, IgE responses were generated frequently by either IgM (mu+/gamma-alpha-) or IgA (alpha +/mu-)-positive B cells (16 and 14% of the Ig producing wells, respectively), but rarely by IgG (gamma +/mu-)-positive B cells (1.3% of Ig producing wells). The total amounts of Ig secreted by IgM-, IgG-, or IgA-positive cells and the total proportions of

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39

Nielsen, Sandra C. A., Krishna M. Roskin, Katherine J. L. Jackson, et al. "Shaping of infant B cell receptor repertoires by environmental factors and infectious disease." Science Translational Medicine 11, no. 481 (2019): eaat2004. http://dx.doi.org/10.1126/scitranslmed.aat2004.

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Antigenic exposures at epithelial sites in infancy and early childhood are thought to influence the maturation of humoral immunity and modulate the risk of developing immunoglobulin E (IgE)–mediated allergic disease. How different kinds of environmental exposures influence B cell isotype switching to IgE, IgG, or IgA, and the somatic mutation maturation of these antibody pools, is not fully understood. We sequenced antibody repertoires in longitudinal blood samples in a birth cohort from infancy through the first 3 years of life and found that, whereas IgG and IgA show linear increases in muta

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40

Микелов, А. И., Д. Б. Староверов, Е. А. Комеч, Ю. Б. Лебедев, Д. М. Чудаков та И. В. Звягин. "Согласованная динамика сывороточного IgE и численности IgE+-клонотипов с уровнем пыльцы в воздухе при поллинозе". Вестник Российского государственного медицинского университета, № 5 (31 жовтня 2019): 14–24. http://dx.doi.org/10.24075/vrgmu.2019.072.

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Механизмы поддержания иммунологической памяти, обусловливающей хроническое течение сезонного аллергического ринита у человека, слабо изучены. Рациональный дизайн новых подходов к терапии аллергических заболеваний требует детального понимания этих механизмов. Известно, что уровень аллергенспецифичных антител класса IgE (sIgE), являющихся ключевым агентом в развитии данного заболевания, повышен у пациентов с поллинозом в период цветения. Целью работы было изучить динамику сывороточного уровня IgE и характеристик клонального репертуара IgE-секретирующих лимфоцитов в зависимости от интенсивности к

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41

Laffer, S., C. Lupinek, I. Rauter, et al. "A high-affinity monoclonal anti-IgE antibody for depletion of IgE and IgE-bearing cells." Allergy 63, no. 6 (2008): 695–702. http://dx.doi.org/10.1111/j.1398-9995.2008.01664.x.

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42

Saunders, Sean P., Sriram Narayanan, Viping N. Narang, et al. "Plasma cells and not memory cells, constitute the majority of human IgE Cells." Journal of Immunology 198, no. 1_Supplement (2017): 135.2. http://dx.doi.org/10.4049/jimmunol.198.supp.135.2.

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Abstract Immunoglobulin E (IgE) is central in allergy pathology as it binds high-affinity receptors on mast cells, inducing degranulation upon allergen crosslinking. However, IgE has the lowest serum concentration and shortest half-life of all Ig’s, and IgE+ B cells are extremely rare. This work aims to uncover characteristics of IgE+B cells that could be used in the design of new therapeutic strategies for allergic diseases. IgE+ cells were identified in Atopic Dermatitis (AD) patients, and were also generated in vitro by stimulating with aCD40 and IL-4. Naïve, IgG+, IgA+ and IgE+ cells from

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43

Mikelov, AI, DB Staroverov, EA Komech, YuB Lebedev, DM Chudakov, and IV Zvyagin. "Correlated dynamics of serum IGE and IGE+ clonotype count with allergen air level in seasonal allergic rhinitis." IMMUNO-ONCOLOGY, no. 5 (October 31, 2019): 13–22. http://dx.doi.org/10.24075/brsmu.2019.072.

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Abstract (sommario):

Mechanisms of maintenance of immunological memory in the chronic course of seasonal allergic rhinitis remain poorly understood. The detailed understanding of these mechanisms is required for design of new approaches for allergy treatment. It is known that the level of allergen-specific IgE antibodies (sIgE), which play a key role in the development of the disease, is increased in patients with seasonal allergic rhinitis during pollination season. This study aimed to investigate the dynamics of serum IgE levels and characteristics of the clonal repertoire of IgE-secreting lymphocytes depending

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44

Sherr, E., E. Macy, H. Kimata, M. Gilly, and A. Saxon. "Binding the low affinity Fc epsilon R on B cells suppresses ongoing human IgE synthesis." Journal of Immunology 142, no. 2 (1989): 481–89. http://dx.doi.org/10.4049/jimmunol.142.2.481.

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Abstract (sommario):

Abstract Our results support the hypothesis that binding the low affinity Fc epsilon R (Fc epsilon R-II, CD23) on IgE-secreting B cells, directly suppresses IgE production. IgE production from AF-10/U266 (a human IgE plasmacytoma) decreased upon incubation with anti-IgE mAb or IgE:anti-IgE immune complexes (IgE-IC). Synthesis was suppressed a maximum of 51% with 10 micrograms/ml of IgE-IC after a 24-h incubation. Spontaneous in vitro IgE synthesis from the B cells of highly atopic individuals was also inhibited in a similar fashion. This effect was isotype specific as IgA or IgG immune complex

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45

Haba, S., and A. Nisonoff. "Effects of syngeneic anti-IgE antibodies on the development of IgE memory and on the secondary IgE response." Journal of Immunology 152, no. 1 (1994): 51–57. http://dx.doi.org/10.4049/jimmunol.152.1.51.

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Abstract The prolonged inhibition of IgE synthesis in mice caused by perinatal inoculation of IgE is attributable, at least in part, to the formation of anti-IgE antibodies. The induction of unresponsiveness with respect to IgE synthesis requires that IgE be administered during a brief interval (2 to approximately 10) days after birth, that corresponds with the time period during which anti-IgE antibodies are induced. Passive administration of syngeneic anti-IgE also inhibits IgE synthesis. We have now investigated the effect of anti-IgE on the induction of memory for IgE production and on sec

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46

Rudolf, M. P., K. Furukawa, S. Miescher, M. Vogel, F. Kricek, and B. M. Stadler. "Effect of anti-IgE antibodies on Fc epsilonRI-bound IgE." Journal of Immunology 157, no. 12 (1996): 5646–52. http://dx.doi.org/10.4049/jimmunol.157.12.5646.

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Abstract Anti-IgE mAbs have always been used to trigger mediator release from basophils or mast cells. Now nonanaphylactogenic anti-human IgE Abs are in clinical evaluation as a therapeutic agent against atopic disease. We have found a mAb that is nonanaphylactogenic but recognizes receptor-bound IgE. Interestingly, the Ab prevents the association of IgE with its receptor if immune complexes were formed between IgE and anti-IgE mAb. This explained the phenomenon that addition of anti-IgE Ab to receptor-bound IgE resulted in a decrease of receptor-bound IgE, because IgE dissociating from the re

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47

Didierlaurent, A., E. Bloch-Michel, M. N. Couret, and H. Susini de Luca. "Tear IgE detected by a new method: Stallerdiag-IgE." Ocular Immunology and Inflammation 2, no. 2 (1994): 93–99. http://dx.doi.org/10.3109/09273949409057065.

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48

Navinés-Ferrer, Arnau, Eva Serrano-Candelas, Gustavo-J. Molina-Molina, and Margarita Martín. "IgE-Related Chronic Diseases and Anti-IgE-Based Treatments." Journal of Immunology Research 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/8163803.

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Abstract (sommario):

IgE is an immunoglobulin that plays a central role in acute allergic reactions and chronic inflammatory allergic diseases. The development of a drug able to neutralize this antibody represents a breakthrough in the treatment of inflammatory pathologies with a probable allergic basis. This review focuses on IgE-related chronic diseases, such as allergic asthma and chronic urticaria (CU), and on the role of the anti-IgE monoclonal antibody, omalizumab, in their treatment. We also assess the off-label use of omalizumab for other pathologies associated with IgE and report the latest findings conce

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Wright, J. D., and C. Lim. "Prediction of an anti-IgE binding site on IgE." Protein Engineering Design and Selection 11, no. 6 (1998): 421–27. http://dx.doi.org/10.1093/protein/11.6.421.

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Lommatzsch, M., K. Geißler, K. C. Bergmann, and J. Virchow. "IgE und Anti-IgE bei Asthma: eine wechselvolle Geschichte." Pneumologie 71, no. 06 (2017): 398–405. http://dx.doi.org/10.1055/s-0043-102070.

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Abstract (sommario):

ZusammenfassungEs war ein langer und verschlungener Weg, der zur Entdeckung von Immunglobulin E (IgE) in den Jahren 1966 und 1967 führte. Wir befinden uns aktuell auf einem langen und verschlungenen Weg, um die immunologische Basis der klinischen Wirkung des Anti-IgE-Antikörpers Omalizumab bei Asthma zu begreifen. Möglicherweise profitieren beim Asthma (ähnlich wie bei der chronisch spontanen Urtikaria) Patienten auf unterschiedliche immunologische Art und Weise von einer Omalizumab-Therapie. Dieser Artikel gibt einen Überblick über die Historie der IgE-Entdeckung und die aktuellen Konzepte de

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