Aspirin-exacerbated respiratory disease: Mediators and mechanisms of a clinical disease - 19/04/17
Doi : 10.1016/j.jaci.2016.09.025
Katherine N. Cahill, MD a, b, Joshua A. Boyce, MD a, b, ⁎ 
a Department of Medicine, Division of Rheumatology, Allergy and Immunology, Brigham and Women's Hospital, Boston, Mass
b Harvard Medical School, Boston, Mass
∗Corresponding author: Joshua A. Boyce, MD, Brigham and Women's Hospital, 1 Jimmy Fund Way, Rm 638, Boston, MA 02115.Brigham and Women's Hospital1 Jimmy Fund WayRm 638BostonMA02115
Key words : Aspirin-exacerbated respiratory disease, cysteinyl leukotrienes, prostaglandin D2, innate immune mechanisms, future targets
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Plan
| Supported by the National Institutes of Health (AI118804, AI078908, AI095219, AT002782, AI082369, HL111113, and HL117945) and by generous contributions from the Vinik Family. |
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| Disclosure of potential conflict of interest: K.N. Cahill has received a grant from the National Institutes of Health. J.A. Boyce declares that he has no relevant conflicts of interest. |
© 2016
Publié par Elsevier Masson SAS.
Vol 139 - N° 3
P. 764-766 - mars 2017 Retour au numéro
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