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Articoli di riviste sul tema "IgE"

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Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 11 marzo 2023

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1

Mastrangelo, G., C. Veller Fornasa, S. Pavanello, G. Marcer, M. Lazzaro, G. Milan, E. Fadda, U. Fedeli e E. Clonfero. "Polyaromatic Hydrocarbons Administered in Humans by Dermal Route Increase Total IgE". International Journal of Immunopathology and Pharmacology 16, n. 2 (maggio 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. Replicated means were compared by analysis of variance for repeated measures and by the Newman-Keuls' test. IgE0, IgE4 and IgE8 were 151.19, 159.69 (a 6% excess) and 170.90 kU/L (a 13% excess) respectively; pairwise comparison showed IgE8 was significantly higher than IgE0 (p<0.05). At multiple linear regression analysis, the percentage increase in serum IgE across observation days was the dependent variable against age, sex, cigarettes/day, urinary 1-pyrenol, atopy, skin area treated, and grams of cream. Of the independent variables, only age had a significant (p<0.028) influence: the younger the age, the higher the IgE response to PAHs. We conclude that whatever the source and the route of entry (skin or respiratory tract), PAHs increase total serum IgE, mainly in younger age groups.

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2

Ledford, Dennis K. "Increased IgE in IgA Deficiency". Journal of Allergy and Clinical Immunology: In Practice 5, n. 6 (novembre 2017): 1795. http://dx.doi.org/10.1016/j.jaip.2017.07.013.

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3

Kolopp-Sarda, M. N., e G. C. Faure. "Pourquoi les immunoglobulines s’appellent-elles IgG, IgA, IgM, IgD et IgE ?" Revue Francophone des Laboratoires 2016, n. 484 (luglio 2016): 57–58. http://dx.doi.org/10.1016/s1773-035x(16)30250-7.

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4

Abbal, Michel. "IgE totales et IgE spécifiques". Bio Tribune Magazine 6, n. 1 (giugno 2003): 20–22. http://dx.doi.org/10.1007/bf03010285.

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5

Corrado, Alessia, Richard P. Ramonell, Matthew C. Woodruff, Christopher Tipton, Sarah Wise, Joshua Levy, John DelGaudio et al. "Extrafollicular IgD+ B cells generate IgE antibody secreting cells in the nasal mucosa". Mucosal Immunology 14, n. 5 (28 maggio 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 predominantly co-express IgM. However, a small but significant fraction co-express IgG or IgA instead which also show connectivity to ASC IgE. Phenotypically, NP IgD+ B cells display an activated profile and molecular evidence of BCR engagement. Transcriptionally, mucosal IgD+ B cells reveal an intermediate profile between naïve B cells and ASC. Single cell IgE ASC analysis demonstrates lower mutational frequencies relative to IgG, IgA, and IgD ASC consistent with IgE ASC derivation from mucosal IgD+ B cell with low mutational load. In conclusion, we describe a novel mechanism of GC-independent, extrafollicular IgE ASC formation at the nasal mucosa whereby activated IgD+ naïve B cells locally undergo direct and indirect (through IgG and IgA), IgE class switch.

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6

Sabra, Aderbal, Joseph A. Bellanti, Jonathan M. Rais, Henry J. Castro, Julia Mendez de Inocencio e Selma Sabra. "IgE and non-IgE food allergy". Annals of Allergy, Asthma & Immunology 90, n. 6 (giugno 2003): 71–76. http://dx.doi.org/10.1016/s1081-1206(10)61664-x.

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7

Boltansky, Howard, Jean Dyer, Steve Esworthy e Michael Kaliner. "IgE-immunotoxins. I. IgE-intact ricin". Immunopharmacology 14, n. 1 (settembre 1987): 35–45. http://dx.doi.org/10.1016/0162-3109(87)90007-5.

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8

Xie, Liping, John T. Schroeder, Jacqueline M. Langdon, Rebecca S. Sora-Scott, Toshiaki Kawakami e Susan M. MacDonald. "Human IgE+ and IgE− are not equivalent to mouse highly cytokinergic IgE". Journal of Allergy and Clinical Immunology 121, n. 4 (aprile 2008): 1027–33. http://dx.doi.org/10.1016/j.jaci.2007.12.1157.

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9

DECLERCK, L., M. WESTEDT, A. CATS, B. VERMEER, E. WELTEVREDEN, C. BRIDTS e W. STEVENS. "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, n. 1 (gennaio 1985): 202. http://dx.doi.org/10.1016/0091-6749(85)90527-5.

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10

Pankovics, Gergő. "Az ige jelentésének összefüggése az igei vonzatstruktúrával". Magyar Nyelvőr 145, n. 2 (2021): 211–19. http://dx.doi.org/10.38143/nyr.2021.2.211.

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11

Adachi, M., N. Noro, T. Nagai e J. Yodoi. "Regulatory mechanism of IgA and IgE production". Annales de l'Institut Pasteur / Immunologie 136, n. 3 (gennaio 1985): 403–6. http://dx.doi.org/10.1016/s0769-2625(85)80014-3.

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12

Nawata, Y., T. Koike, H. Hosokawa, H. Tomioka e S. Yoshida. "Anti-IgE autoantibody in patients with atopic dermatitis." Journal of Immunology 135, n. 1 (1 luglio 1985): 478–82. http://dx.doi.org/10.4049/jimmunol.135.1.478.

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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 with self IgE. The role of the IgE-anti-IgE immune complex and the role of the anti-IgE autoantibody in the modulation of the IgE-mediated immune system in atopic dermatitis are discussed.

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13

Marinkovich, Vincent A., e Neil Woodmansey. "Total IgE and Allergen-Specific IgE Assays". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 25, n. 2 (marzo 1988): 195–96. http://dx.doi.org/10.1177/000456328802500214.

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14

Boltansky, Howard, Jay Slater, Richard Youle, Chaviva Isersky e Michael Kaliner. "IgE-immunotoxins. II. IgE-ricin A-chain". Immunopharmacology 14, n. 1 (settembre 1987): 47–62. http://dx.doi.org/10.1016/0162-3109(87)90008-7.

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15

Vassella, Claudia C., Alain L. de Weck e Beda M. Stadler. "Influence of IgE Fragments on IgE Determination". International Archives of Allergy and Immunology 92, n. 3 (1990): 272–80. http://dx.doi.org/10.1159/000235189.

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16

Nakajima, T., M. Sarfati e G. Delespesse. "Relationship between human IgE-binding factors (IgE-BF) and lymphocyte receptors for IgE." Journal of Immunology 139, n. 3 (1 agosto 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 the CSN of molecules reacting with two MabER. 3) Surface radioiodinated tonsillar lymphocytes or RPMI 8866 cells release labeled IgE-binding molecules displaying the same antigenic composition and the same migration on SDS-PAGE as purified IgE-BF. 4) Peptide mapping of highly purified IgE-BF and Fc epsilon R reveals the presence of several identical fragments after digestion with either alpha-chymotrypsin, trypsin, or papain. Moreover, papain digestion of the 25-27 kD IgE-BF and of the affinity-purified Fc epsilon R, generated a 15 kD fragment reacting with two MabER and that is known to bind IgE. Although these data strongly suggest that IgE-BF may be directly derived from cell surface IgE receptors, they do not exclude the possibility that some IgE-BF may also be secreted without being first anchored in the cell membrane.

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17

Harfi, Harb A., e John T. Godwin. "Normal Serum Levels of IgG, IgA, IgM, IgD, and IgE in Saudi Arabia". Annals of Saudi Medicine 5, n. 2 (aprile 1985): 99–104. http://dx.doi.org/10.5144/0256-4947.1985.99.

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18

Salonen, Eeva-Marjatta, Tapani Hovi, Olli Meurman, Timo Vesikari e Antti Vaheri. "Kinetics of specific IgA, IgD, IgE, IgG, and IgM antibody responses in rubella". Journal of Medical Virology 16, n. 1 (maggio 1985): 1–9. http://dx.doi.org/10.1002/jmv.1890160102.

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19

Novak, Natalija, Stefan Kraft e Thomas Bieber. "IgE receptors". Current Opinion in Immunology 13, n. 6 (dicembre 2001): 721–26. http://dx.doi.org/10.1016/s0952-7915(01)00285-0.

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20

Josephs, Debra H., James F. Spicer, Panagiotis Karagiannis, Hannah J. Gould e Sophia N. Karagiannis. "IgE immunotherapy". mAbs 6, n. 1 (4 novembre 2013): 54–72. http://dx.doi.org/10.4161/mabs.27029.

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21

Hegewisch, S., K. Mainzer e D. Braumann. "IgE myelomatosis". Blut 55, n. 1 (luglio 1987): 55–60. http://dx.doi.org/10.1007/bf00319644.

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22

Delespesse, G., M. Sarfati e C. Heusser. "IgE synthesis". Current Opinion in Immunology 2, n. 4 (aprile 1990): 506–12. http://dx.doi.org/10.1016/0952-7915(90)90003-y.

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23

ROBBANA-BARNAT, SAIDA, e JACQUES FRADIN. "Cereal Grains: IgE- and Non-IgE-mediated Reactions". Journal of Nutritional & Environmental Medicine 7, n. 1 (gennaio 1997): 35–46. http://dx.doi.org/10.1080/13590849762781.

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24

Bloch-Michel, E., S. Liotet, M. P. Lecorvec e P. M. Cerqueti. "IgE des larmes, IgE sériques et tests cutanés". Revue Française d'Allergologie et d'Immunologie Clinique 25, n. 3 (luglio 1985): 135–39. http://dx.doi.org/10.1016/s0335-7457(85)80014-9.

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25

de Macario, Everly Conway, A. J. L. Macario e R. J. Jovell. "Slide immunoenzymatic assay for human IgE (SIA-IgE)". Journal of Immunological Methods 90, n. 1 (giugno 1986): 137–41. http://dx.doi.org/10.1016/0022-1759(86)90394-7.

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26

Platzer, Barbara, Floortje Ruiter, John van der Mee e Edda Fiebiger. "Soluble IgE receptors—Elements of the IgE network". Immunology Letters 141, n. 1 (dicembre 2011): 36–44. http://dx.doi.org/10.1016/j.imlet.2011.08.004.

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27

Haniuda, Kei, Saori Fukao, Tadahiro Kodama, Hitoshi Hasegawa e Daisuke Kitamura. "Autonomous membrane IgE signaling prevents IgE-memory formation". Nature Immunology 17, n. 9 (18 luglio 2016): 1109–17. http://dx.doi.org/10.1038/ni.3508.

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28

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

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29

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

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30

Delespesse, G., e M. Sarfati. "IgE-binding factors (soluble CD23) and IgE regulation". Research in Immunology 141, n. 1 (1990): 75–77. http://dx.doi.org/10.1016/0923-2494(90)90105-8.

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31

Ando, Tomoaki, e Jiro Kitaura. "Tuning IgE: IgE-Associating Molecules and Their Effects on IgE-Dependent Mast Cell Reactions". Cells 10, n. 7 (5 luglio 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-threatening allergic diseases, such as asthma and anaphylaxis. Therefore, reactivity of the IgE sensor is fine-tuned by various IgE-associating molecules. In this review, we discuss the mechanistic basis for how IgE-dependent mast cell activation is regulated by the IgE-associating molecules, including the newly developed therapeutic candidates.

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32

Haba, S., e 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, n. 9 (1 maggio 1990): 3363–67. http://dx.doi.org/10.1073/pnas.87.9.3363.

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33

Ezeamuzie, Charles I., Raja'a Al-Attiyah, Puthiyaveetil K. Shihab e 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, n. 9 (agosto 2009): 1110–14. http://dx.doi.org/10.1016/j.intimp.2009.05.009.

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34

Laffer, S., C. Lupinek, I. Rauter, M. Kneidinger, A. Drescher, J. H. Jordan, M. T. Krauth et al. "A high-affinity monoclonal anti-IgE antibody for depletion of IgE and IgE-bearing cells". Allergy 63, n. 6 (giugno 2008): 695–702. http://dx.doi.org/10.1111/j.1398-9995.2008.01664.x.

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35

Didierlaurent, A., E. Bloch-Michel, M. N. Couret e H. Susini de Luca. "Tear IgE detected by a new method: Stallerdiag-IgE". Ocular Immunology and Inflammation 2, n. 2 (gennaio 1994): 93–99. http://dx.doi.org/10.3109/09273949409057065.

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36

Navinés-Ferrer, Arnau, Eva Serrano-Candelas, Gustavo-J. Molina-Molina e 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 concerning this drug and other new related drugs. To date, omalizumab has only been approved for severe allergic asthma and unresponsive chronic urticaria treatments. In allergic asthma, omalizumab has demonstrated its efficacy in reducing the dose of inhaled corticosteroids required by patients, decreasing the number of asthma exacerbations, and limiting the effect on airway remodeling. In CU, omalizumab treatment rapidly improves symptoms and in some cases achieves complete disease remission. In systemic mastocytosis, omalizumab also improves symptoms and its prophylactic use to prevent anaphylactic reactions has also been discussed. In other pathologies such as atopic dermatitis, food allergy, allergic rhinitis, nasal polyposis, and keratoconjunctivitis, omalizumab significantly improves clinical manifestations. Omalizumab acts in two ways: by sequestering free IgE and by accelerating the dissociation of the IgE-Fcεreceptor I complex.

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37

Wright, J. D., e C. Lim. "Prediction of an anti-IgE binding site on IgE". Protein Engineering Design and Selection 11, n. 6 (1 giugno 1998): 421–27. http://dx.doi.org/10.1093/protein/11.6.421.

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38

Lommatzsch, M., K. Geißler, K. C. Bergmann e J. Virchow. "IgE und Anti-IgE bei Asthma: eine wechselvolle Geschichte". Pneumologie 71, n. 06 (giugno 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 der Anti-IgE-Therapie bei Asthma.

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39

Larsen, Carsten S., Mette Christiansen e Trine H. Mogensen. "Autosomal Dominant Hyper-IgE Syndrome Without Significantly Elevated IgE". Journal of Clinical Immunology 39, n. 8 (29 agosto 2019): 827–31. http://dx.doi.org/10.1007/s10875-019-00683-8.

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40

Hamelmann, E., C. Rolinck-Werninghaus e U. Wahn. "From IgE to Anti-IgE: Where do we stand?" Allergy 57, n. 11 (novembre 2002): 983–94. http://dx.doi.org/10.1034/j.1398-9995.2002.02165.x.

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41

Yilmaz, H., K. L. Morgan e J. M. Roe. "Cross-Reactivity of Ovine IgE with Anti-Human IgE". International Archives of Allergy and Immunology 104, n. 3 (1994): 277–80. http://dx.doi.org/10.1159/000236677.

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42

Aouthmany, A., F. Hsieh e R. Burton. "FACTORS INFLUENCING SERUM IGE VARIABILITY AND SECONDARY IGE DEFICIENCY". Annals of Allergy, Asthma & Immunology 129, n. 5 (novembre 2022): S54. http://dx.doi.org/10.1016/j.anai.2022.08.651.

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43

Chen, Swey-Shen Alex. "Genesis of host IgE competence: perinatal IgE tolerance induced by IgE processed and presented by IgE Fc receptor (CD23)-bearing B cells". European Journal of Immunology 22, n. 2 (febbraio 1992): 343–48. http://dx.doi.org/10.1002/eji.1830220209.

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44

Zhang, X. H., C. Werner-Favre, H. Y. Tang, N. Brouwers, J. Y. Bonnefoy e R. H. Zubler. "IL-4-dependent IgE switch in membrane IgA-positive human B cells." Journal of Immunology 147, n. 9 (1 novembre 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 responding autoclone wells (23-27%) were comparable. All IgE secretion was IL-4 dependent. When the Ig secretion patterns from alpha +/mu- vs alpha +/mu-epsilon- B cells were compared, most autoclone wells from both types of cells produced IgA only, and similar proportions of IgA producing wells (6.2 and 6.0%) also secreted IgE. In addition, IgE restricted responses occurred 6 times more frequently with alpha +/mu- than with alpha +/mu-epsilon- cells, which suggests that membrane IgA+E double-positive, IgE committed B cells occur in vivo. The isotype pattern generated by alpha +/mu-epsilon- B cells cannot be explained by a chance assortment of separate IgA and IgE precursors or by cytophilic antibody. Thus, IL-4 dependent switch to IgE occurred frequently in IgM- or IgA-positive, but rarely among total IgG-positive, B cells. This could be relevant to IgE production in mucosal tissues rich in IgA expressing B cells.

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45

Ishizaka, K. "Twenty years with IgE: from the identification of IgE to regulatory factors for the IgE response." Journal of Immunology 135, n. 1 (1 luglio 1985): i. http://dx.doi.org/10.4049/jimmunol.135.1.i.

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46

Shiung, Yu-Yu, Chen-Yi Chiang, Jiun-Bo Chen, Pheidias Wu, Alfur Hung e Tse Wen Chang. "Anti-IgE monoclonal antibodies that bind to IgE bound by CD23 but not to IgE bound by IgE Fc receptors on basophils (86.10)". Journal of Immunology 184, n. 1_Supplement (1 aprile 2010): 86.10. http://dx.doi.org/10.4049/jimmunol.184.supp.86.10.

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Abstract (sommario):

Abstract IgE is a central mediator responsible for immediate-type hypersensitivity reactions. The anti-IgE monoclonal antibody (mAb), omalizumab, has been shown in numerous clinical trials to be efficacious in the treatment of severe allergic asthma and other allergic diseases. Omalizumab was designed to bind to free IgE in blood and membrane-bound IgE (mIgE) on B cells, but not to IgE bound by the high-affinity IgE Fc receptors (FcϵRI) on basophils and mast cells and by the low-affinity IgE Fc receptors (CD23) on B cells and many other cell types. Additionally, omalizumab can bind to IgE and prevent it from binding to both FcϵRI and CD23. Studies by other groups have also shown that CD23 is involved in the synthesis of IgE and that interfering CD23 function, such as by cross-linking CD23 on B cell surface, can cause the down-regulation of IgE production. We have developed anti-IgE mAbs that mimic omalizumab in various aspects except their ability to bind to IgE on CD23. These newly developed mAbs bind to linear epitopes on IgE. They do not induce the degranulation of IgE-pulsed rat basophilic leukemic cells (RBL SX-38), which had been transfected with the genes of human FcϵRI. The ability of the mAbs to cross-link IgE-occupied CD23 on the cell surface of B cell lines is being tested. The results suggest that these anti-IgE mAbs may render a set of pharmacological mechanisms, which are somewhat different from that of omalizumab, for controlling IgE in patients with allergic diseases.

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47

Śpiewak, Radosław. "Hyper-IgE syndrome". Dermatopedia 3 (2014): 003. http://dx.doi.org/10.14320/dermatopedia.pl.2014.003.

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48

Nielsen, Sandra C. A., Krishna M. Roskin, Katherine J. L. Jackson, Shilpa A. Joshi, Parastu Nejad, Ji-Yeun Lee, Lisa E. Wagar et al. "Shaping of infant B cell receptor repertoires by environmental factors and infectious disease". Science Translational Medicine 11, n. 481 (27 febbraio 2019): eaat2004. http://dx.doi.org/10.1126/scitranslmed.aat2004.

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Abstract (sommario):

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 mutational maturation with age, IgM and IgD mutations are more closely tied to pathogen exposure. IgE mutation frequencies are primarily increased in children with impaired skin barrier conditions such as eczema, suggesting that IgE affinity maturation could provide a mechanistic link between epithelial barrier failure and allergy development.

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49

Furukawa, Takatoshi, Yuji Takada, Hironobu Asao, Nobuo Ohta e Seiji Kakehata. "Hyper-IgE syndrome". Journal of Japan Society of Immunology & Allergology in Otolaryngology 36, n. 4 (2018): 267–69. http://dx.doi.org/10.5648/jjiao.36.267.

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50

Rezaei, N., e A. Aghamohammadi. "Hyper-IgE syndrome". Journal of Postgraduate Medicine 56, n. 2 (2010): 63. http://dx.doi.org/10.4103/0022-3859.65271.

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