Pathogenic and protective roles of B cells and antibodies in patients with chronic rhinosinusitis - 04/05/18
Abstract |
Chronic rhinosinusitis (CRS) is a chronic inflammatory disease of the nose and sinuses that affects up to 12% of the population in Europe and the United States. This complex disease is likely driven by multiple environmental, genetic, and inflammatory mechanisms, and recent studies suggest that B cells might play a critical role in disease pathogenesis. B cells and their antibodies have undisputed roles in health and disease within the airway mucosae. Deficient or inadequate B-cell responses can lead to susceptibility to infectious disease in the nose, whereas excess antibody production, including autoantibodies, can promote damaging inflammation. Thus, patients with B-cell defects often have either chronic or recurrent acute infections, and this can be associated with nonpolypoid CRS. In contrast, many patients with CRS with nasal polyps, which is less likely to be driven by pathogens, have excess production of local immunoglobulins, including autoreactive antibodies. These B-cell responses activate complement in many patients and likely contribute to immunopathogenic responses. A better understanding of the B cell–associated mechanisms that drive disease in patients with CRS should be a high priority in the quest to understand the pathogenesis of this disease.
Le texte complet de cet article est disponible en PDF.Key words : Antibodies, antibody deficiency, autoimmunity, chronic rhinosinusitis, B cells, immunodeficiency, mucosal immunity
Abbreviations used : BAFF, BAFF-R, CRS, CRSsNP, CRSwNP, CVID, EBI2, GC, GPA, ICOS, NF-κB, sIgA, SLO, TACI, TLO
Plan
Supported by National Institutes of Health grants R56 AI121239, U19 AI106683, and R01 AI072570 and the Ernest S. Bazley Trust. |
|
Disclosure of potential conflict of interest: B. K. Tan received grant U19 AI106683 from the National Institutes of Health (NIH) and personal fees from P-value Communications, Premier Healthcare, and the American Academy of Allergy, Asthma & Immunology. R. P. Schleimer's institution and he both received a grant from the NIH for this work, and he received personal fees from Intersect ENT, GlaxoSmithKline, Allakos, Merck, Sanofi, AstraZeneca/Medimmune, Genentech, and Otsuka; received consultancy fees from Intersect ENT, GlaxoSmithKline, Allakos, Sanofi, AstraZeneca/Medimmune, BioMarck, Exicure, Aqualung Therapeutics, and Ostuka; received stock options form Auransense, BioMarck, Exicure, and Aqualung Therapeutics; and had a patent issued and licensed by Allakos (Siglec-8 and Siglec-8 ligand–related patents). K. E. Hulse received a grant from the NIH for this work. A. T. Peters declares she has no relevant conflicts of interest. |
|
Terms in boldface and italics are detailed in the glossary on page 1554. |
Vol 141 - N° 5
P. 1553-1560 - mai 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Déjà abonné à cette revue ?