Immune response modifiers in the treatment of asthma: A PRACTALL document of the American Academy of Allergy, Asthma & Immunology and the European Academy of Allergy and Clinical Immunology
Article Outline
- IRMs that neutralize effector molecules
- IRMs that affect the TH2 pathway
- Interruption of the IL-4, IL-13, and IL-4Rα pathways
- Anti–IL-5
- Modulation of the chemoattractant receptor-homologous molecule expressed on TH2 cells receptor
- Antagonists of adhesion and chemokine pathways controlling eosinophil and TH2 lymphocyte migration
- IL-9 and more recently described TH2-associated cytokines
- Inhibition of T cells and their coreceptors
- IRMs that affect signaling pathways
- Peroxisome proliferator-activated receptor agonists
- IRMs as adjuvants for allergen immunotherapy
- Adverse events of IRMs
- The future of IRMs
- Summary
- References
- Copyright
Abbreviations used: APC, Antigen-presenting cell, CRTH2, Chemoattractant receptor-homologous molecule expressed on TH2 cells (also known as DP2), FDA, US Food and Drug Administration, Feno, Fraction of exhaled nitric oxide, IL-4R, IL-4 receptor, IRM, Immune response modifier, MPLA, Monophosphoryl lipid A, PAMP, Pathogen-associated molecular pattern, PPAR, Peroxisome proliferator-activated receptor,Syk, Spleen tyrosine kinase, TKI, Tyrosine kinase inhibitor, TLR, Toll-like receptor, VLA-4, Very late antigen 4
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