Unraveling the complexity of leukotriene and prostaglandin inflammatory signaling - 07/01/16
Doi : 10.1016/j.jaci.2015.09.003
Efren Rael, MD, FAAAAI ⁎ 
Sean N. Parker Center for Allergy and Asthma Research, Mountain View, and the Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, and the California Pacific Medical Clinical Center for Allergy and Immunology, Stanford University, Stanford, Calif
∗Corresponding author: Efren Rael, MD, FAAAAI, Sean N. Parker Center for Allergy and Asthma Research, Stanford University, 2500 Grant Rd, El Camino Hospital, 4th Floor, Tower C, Mountain View, CA 94040.
Key words : Asthma, diabetes, obesity, hyperlipidemia, nasal polyps, aspirin-exacerbated respiratory disease, allergic rhinitis, prostaglandin E2, leukotriene D4, cysteinyl leukotriene receptor 1, prostaglandin E receptor 3, prostaglandin D2, mast cells, translational research
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| Disclosure of potential conflict of interest: The author declares that he has no relevant conflicts of interest. |
© 2015
American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
Vol 137 - N° 1
P. 299-300 - janvier 2016 Retour au numéro
Article précédent
- Leukotriene D4 and prostaglandin E2 signals synergize and potentiate vascular inflammation in a mast cell–dependent manner through cysteinyl leukotriene receptor 1 and E-prostanoid receptor 3
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