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• W2140231084 abstract "Phagocytes are part of the mononuclear phagocyte system that represents a key component of innate and adaptive immunity. They are armed with a variety of PRRs and have the capability to produce reactive oxygen species rapidly and release preformed antimicrobial molecules. Prevention of infection and assuring appropriate tissue turnover by removal of dead cells are the primary roles of the innate immune system. It is therefore conceivable that dysfunction of even one of its many components can cause disease, as demonstrated by the fairly large number of primary immunodeficiency diseases, in which genetic defects provoke a variety of microbial infections [1]. How lungs balance the delicate barrier to inhaled intruders and an excessive inflammatory response has been studied for decades and has allowed for the recognition that myeloid cells, in a pulmonary microenvironment, acquire unique regulatory mechanisms. Furthermore, the role of the SR for maintenance of lung homeostasis appears critical [2–4]. CF is a leading genetic cause of mortality among Caucasians [5]. It is primarily a disorder of electrolyte transport by epithelial cells, in which an anion channel activated by cAMP–dependent kinase is defective (CFTR). Mutations in the CFTR gene result in variants that are unstable, mislocalized, or have altered Cl− conductance [6]. The role of macrophages in CF and in particular, of those resident in the lung (PAM) is poorly understood, despite considerable research efforts and their critical role in lungs, a primary therapeutic target of CF. These cells can display different functional phenotypes, many of which are antagonistic, under the influence of specific mediators. In fact, it is well known that these cells can shift phenotypes from pro– to anti–inflammatory, immunogenic to tolerogenic, and tissue–destructive to tissue–regenerative [7, 8]. This plasticity led to the suspicion that protocols used for their isolation may alter their phenotype and response, thus altering the interpretation attributed to their role in disease [9]." @default.
• W2140231084 created "2016-06-24" @default.
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• W2140231084 date "2009-09-01" @default.
• W2140231084 modified "2023-09-24" @default.
• W2140231084 title "Editorial: The role of macrophages and their scavenger receptors in cystic fibrosis" @default.
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• W2140231084 doi "https://doi.org/10.1189/jlb.0309120" @default.
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