Synthesis of interleukin-1 receptor antagonist by @entity3512 + and @entity3512 - XXXX lung fibroblast subsets.

@entity82 @entity55 @entity19 @entity635 @entity3794 @entity3512 @entity18995
IL-1 is a key cytokine that promotes @entity55 and @entity82 , as a result of its ability to stimulate lung fibroblast proliferation and collagen synthesis, two hallmarks of @entity82 . The @entity18995 ( @entity18995 ) is an important natural inhibitor of IL-1-mediated functions. In models of @entity3794 induced by chemotherapeutic agents or noxious particles, administration of @entity18995 significantly ameliorates lung @entity82 . Lung tissue undergoing an inflammatory response shows elevations in @entity18995 , although it is not clear which pulmonary cells are responsible for the @entity18995 synthesis. The purpose of this research was to determine whether @entity3512 + and @entity3512 - subsets of @entity19 lung fibroblasts were capable of synthesizing @entity18995 . In this report, it is demonstrated for the first time that lung fibroblasts are capable of synthesizing @entity18995 . Both @entity3512 + and @entity3512 - parental lines and clones constitutively express @entity18995 mRNA. Quantitation of @entity18995 protein indicates that @entity3512 + and @entity3512 - fibroblasts secrete similar levels of secreted but not intracellular @entity18995 . @entity3512 - fibroblasts accumulate higher levels of @entity18995 intracellularly. Moreover, fibroblast-conditioned supernatants containing @entity18995 significantly suppress the mitogenic response of a T cell clone, D10G4.1, to concanavalin A and @entity635 . Overall, our observations indicate that @entity3512 + and @entity3512 - fibroblasts release @entity18995 and possess an IL-1-specific inhibitory activity in their supernatants. In vivo, fibroblast-derived @entity18995 may serve to regulate IL-1-mediated effects in an autocrine and/or paracrine fashion to maintain homeostasis in the pulmonary interstitium.
