Identification of receptors and pathways through which LTE 4 exerts its effects may be highly significant in terms of the pathobiology of mucosal inflammation, as well as the treatment of asthma, AERD, and related diseases in which local concentrations of LTE 4 are elevated and/or end-organ reactivity to LTE 4 is high.
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Leukotriene E4-induced pulmonary inflammation is mediated by the P2Y12 receptor.
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