Omalizumab efficacy in cases of chronic spontaneous urticaria is not explained by the inhibition of sera activity in effector cells
Serrano-Candelas E (1,2), Martínez-Aranguren R (3), Vega O (3), Gastaminza G (3), Bartra J (4), Audicana MT (5), Núñez-Córdoba JM (6), Algorta J (7), Valero A (4,8), Martin M (9,10), Ferrer M (11).
(1) Biochemistry Unit, Faculty of Medicine, University of Barcelona, Casanova 143, Barcelona, 08036, Spain.
(2) Laboratory of Clinical and Experimental Respiratory Immunoallergy, IDIBAPS, Barcelona, Spain.
(3) Department of Allergy and Clinical Immunology, Clinica Universidad de Navarra, Pamplona, Spain.
(4) Department of Pneumology and Allergology, Immunoallèrgia Respiratòria Clínical Experimental, IDIBAPS, Hospital Clínic, Barcelona, Spain.
(5) Allergy Service, Hospital Santiago, Vitoria, Spain.
(6) Research Support Service, Central Clinical Trials Unit, Clinica Universidad de Navarra, Pamplona, Spain.
(7) Department of Biochemistry and Molecular Biology, Universidad del Pais Vasco-EHU, Bizkaia, Spain.
(8) Centro de Investigación Biomédica en Red de Enfermedades Respiratorias [Biomedical Research Networking Centre on Respiratory Diseases (CIBERES)], Madrid, Spain.
(9) Biochemistry Unit, Faculty of Medicine, University of Barcelona, Casanova 143, Barcelona, 08036, Spain.
(10) Laboratory of Clinical and Experimental Respiratory Immunoallergy, IDIBAPS, Barcelona, Spain.
(11) Department of Allergy and Clinical Immunology, Clinica Universidad de Navarra, Pamplona, Spain.
Data: 21/Ago/2017Alergologia e Imunologia Clínica
Omalizumab (OmAb) is a humanized anti-IgE antibody approved for the treatment of chronic spontaneous urticaria (CSU).
OmAb's mechanism of action is known to include actions on free IgE and on pre-bound IgE. However, OmAb is equally and rapidly effective against autoimmune and non-autoimmune urticaria where IgE involvement is not clear, suggesting the involvement of additional mechanisms of action.
In this study, we sought to investigate the ability of OmAb to inhibit mast cell and basophil degranulation induced by sera from CSU patients. For this purpose, we performed a comparison between the in vitro incubation of sera from CSU patients treated with OmAb and the in vivo administration of OmAb in a clinical trial.
We found that OmAb added in vitro to sera from CSU patients did not modify the ability of the sera to induce cell degranulation. Similarly, the sera from patients treated with OmAb in the context of the clinical trial who had a good clinical outcome maintained the capacity to activate mast cells and basophils.
Thus, we conclude that the beneficial activity of OmAb does not correlate with the ability of patient sera to induce cell degranulation.
CITAÇÃO DO ARTIGO Sci Rep. 2017 Aug 21;7(1):8985. doi: 10.1038/s41598-017-09361-4
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