Volume 115, Issue 5 , Pages 953-959, May 2005
Allergy and asthma
Initiation and regulation of allergic inflammation is influenced by many factors, including cell type, membrane receptors, and mediators generated. Furthermore, the altered response of targeted tissues (ie, airway smooth muscle) becomes important to the eventual expression of asthma. Finally, the genetic regulation and association of genetic polymorphisms has enhanced our understanding of host susceptibility. In this review key findings published in 2004 issues of the Journal of Allergy and Clinical Immunology are highlighted to demonstrate recent advances in these areas.
Key words: Eosinophils, mast cells, airway smooth muscle, cysteinyl leukotrienes, asthma
Abbreviations used: BAL, Bronchoalveolar lavage, CTLA, Cytotoxic T-lymphocyte antigen, EDN, Eosinophil-derived neutrophil, eNO, Exhaled nitric oxide, EP, E prostanoid, ITIM, Tyrosine-based inhibitory motif, MIP, Macrophage inflammatory protein, NO, Nitric oxide, OX40L, OX40 ligand, PG, Prostaglandin, SNP, Single nucleotide polymorphism, TLR, Toll-like receptor, VEGF, Vascular endothelial growth factor
Disclosure of potential conflict of interest: B. Bochner is a paid consultant for Amgen, Aventis, and GlaxoSmithKline and a codiscoverer with GlaxoSmithKline of Siglec-8, for which they share a patent; he is on the Speakers' Bureau for Merck, Genentech, and Novartis; and he is on advisory boards for Pfizer and Glycomimetics, Inc. W. W. Busse has consultant arrangements with Bristol-Meyers Squibb, Dynavax, Hoffman Laroche, and Fujisawa; has received grants–research support from GlaxoSmithKline, Fujisawa, Aventis, Hoffman Laroche, and Pfizer; is on the speakers' bureau for Merck, GlaxoSmithKline, and Aventis; and is on advisory boards for GlaxoSmithKline, Aventis, Pfizer, and AstraZeneca.
PII: S0091-6749(05)00426-4
doi:10.1016/j.jaci.2005.02.032
© 2005 American Academy of Allergy, Asthma and Immunology. Published by Elsevier Inc. All rights reserved.
Volume 115, Issue 5 , Pages 953-959, May 2005
