I have a longstanding interest in myeloid cells, mononuclear phagocytes and inflammation. Over more than 50 years these interests have, and do, include mechanisms of induction of the inflammatory process and in particular of its regulation and resolution, as well as defects in this that are associated with longer-term sequelae such as tissue remodeling, fibrosis, persistent injury and enhanced or deranged immunological responses. An emphasis on mononuclear phagocyte (monocyte, macrophage and dendritic cell) participation in these processes demonstrated roles and mechanisms for recognition and removal of apoptotic cells and tissue debris after injury and inflammation. Cell removal also occurs in normal cell turnover and maintenance of tissue homeostasis - by mechanisms we termed "efferocytosis" and showed to involve recognition of phosphatidylserine (PS) exposed on apoptotic cells as a result loss of membrane phospholipid asymmetry. In general these cell removal processes were shown to be accompanied by inflammosuppressive mediators that minimize tissue responses and lead to resolution of inflammation as well as active contribution to tissue remodeling and ideally, return to normal structure and function. Equally important were related studies of monocyte/macrophage programing towards a variety of reparative, tissue-modifying and immunomodulatory functions. These in turn were shown to be major players resolution of inflammation and return of tissues to normal structure and function, but also can contribute to abnormal repair as in fibrosis. Thus our studies have consistently addressed mechanisms and signal pathways involved in vivo during inflammation and fibroproliferative responses especially in the respiratory tract. Our research and translational interests in this regard have included ARDS, COPD, Asthma, airways inflammation and interstitial lung diseases (ILD), especially IPF.