STAT3 and suppressor of cytokine signaling 3: potential targets in lung inflammatory responses

Abstract

The expanding knowledge involving the cytokine transcription factor network has provided new insights into the acute lung inflammatory response. There are numerous lung inflammatory diseases that at present lack effective treatment (adult respiratory distress syndrome, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, asthma and so on). Although cytokines themselves and their receptors comprise a communication system that is crucial to detect the presence of pathogens and the injured lung, the cytokine signals and the milieu that surrounds these signals can clearly determine the nature of the lung responses that are elicited. Functioning as a transcription factor, STAT3 participates in the signaling pathways for many cytokines in various cells and organs that are regulated by the suppressor of cytokine signaling (SOCS) family, including SOCS3. Recently, data on the activation and function of STAT3 and SOCS3 in the lung during the acute inflammatory response are emerging, suggesting that these molecules can be potential targets for regulating pulmonary inflammatory responses. The authors review the progress in understanding how STAT3 and SOCS3 regulate the lung inflammatory response.