Immune system dysregulation in chronic lung disease

Chronic lung diseases (CLDs), including chronic obstructive pulmonary disease (COPD), asthma, lung cancer, interstitial lung disease and pulmonary hypertension, present a significant and rising global health problem. CLDs develop at the interface between genetic susceptibilities and environmental aspects, and are currently the second leading cause of death worldwide. Thus far, therapies of only limited effect exist for CLDs; the search for novel and effective therapeutic strategies has been at the centre of recent major research efforts. As part of the pathogenesis of many CLDs, ill-defined lung injuries and failed repair mechanisms ultimately lead to perturbed lung architecture that is incompatible with normal respiratory function. In particular, the immunological mechanisms that initiate and maintain CLD remain to be fully unravelled. The mission of the European Respiratory Society (ERS) is to alleviate suffering from respiratory disease and promote lung health through research, knowledge sharing, and medical and public education. In support of this mission, the ERS holds an annual Lung Science Conference (LSC), which brings together leading basic scientists with physician scientists and clinicians on distinct topics that are of relevance to respiratory medicine. In April 2011, world-leading scientists and clinicians met at the ninth LSC in Estoril, Portugal, to share their latest discoveries and to work towards identifying the cellular and molecular pathways that underlie the development of CLDs. The meeting highlighted major novel findings in immune system (dys)function in the major CLDs, as outlined in detail below. Some of the presentations discussed can be found in the E-Resources on the ERS website (at http://www.ers-education.org/pages/default.aspx?id=2556). The incidence of asthma has been steadily increasing in recent decades and intensive research has particularly focused upon the role of T-helper cell (Th) type 2 responses and therapies designed to neutralise the activity of Th2-associated cytokines, such as interleukin (IL)-4, IL-5 and IL-13. Disappointing …