IL-1β Augments TNF-α–Mediated Inflammatory Responses from Lung Epithelial Cells


Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) mediate the development of numerous infl ammatory lung diseases. Since IL-1β is typically activated in situations where TNF-α is produced, it was hypothesized that IL-1β alters TNF-α–induced proinfl ammatory epithelial cell function by altering TNF receptor shedding and surface abundance. In this… (More)


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