Macrophages in lung fibrosis

International Immunology, Journal Year: 2021, Volume and Issue: 33(12), P. 665 - 671

Published: July 15, 2021

Abstract Pulmonary fibrosis (PF) is a disease in which excessive extracellular matrix (ECM) accumulation occurs the lungs, induces thickening of alveolar walls, ultimately leading to destruction structures and respiratory failure. Idiopathic PF, cause unknown, has poor prognosis with median survival 2–4 years after diagnosis. There currently no known curative treatment. The mechanism underlying PF thought be initiated by dysfunction type II epithelial cells, leads ECM overproduction through activation fibroblasts. In addition, it been suggested that variety cells contribute fibrotic processes. particular, clinical basic research findings examining roles macrophages suggest they may pivotal regulators PF. this review, we discuss characteristics, functions origins subsets involved including resident alveolar, interstitial monocyte-derived macrophages.

Language: Английский

---

Neuropilin-1 mediates lung tissue-specific control of ILC2 function in type 2 immunity

Nature Immunology, Journal Year: 2022, Volume and Issue: 23(2), P. 237 - 250

Published: Jan. 24, 2022

Group 2 innate lymphoid cells (ILC2s) are highly heterogeneous tissue-resident lymphocytes that regulate inflammation and tissue homeostasis in health disease. However, how these integrate into the microenvironment to perform tissue-specific functions is unclear. Here, we show neuropilin-1 (Nrp1), which induced postnatally sustained by lung-derived transforming growth factor beta-1 (TGFβ1), a marker of lung ILC2s. Genetic ablation or pharmacological inhibition Nrp1 suppresses IL-5 IL-13 production ILC2s protects mice from development pulmonary fibrosis. Mechanistically, TGFβ1-Nrp1 signaling enhances ILC2 function type immunity upregulating IL-33 receptor ST2 expression. These findings identify as regulator lung-resident highlight potential therapeutic target for

Language: Английский

---

The role of lung macrophages in acute respiratory distress syndrome

Inflammation Research, Journal Year: 2022, Volume and Issue: 71(12), P. 1417 - 1432

Published: Oct. 20, 2022

Language: Английский

---

Spatiotemporal Adaptations of Macrophage and Dendritic Cell Development and Function

Annual Review of Immunology, Journal Year: 2022, Volume and Issue: 40(1), P. 525 - 557

Published: Feb. 7, 2022

Macrophages and conventional dendritic cells (cDCs) are distributed throughout the body, maintaining tissue homeostasis tolerance to self orchestrating innate adaptive immunity against infection cancer. As they complement each other, it is important understand how cooperate mechanisms that integrate their functions. Both exposed commensal microbes, pathogens, other environmental challenges differ widely among anatomical locations over time. To adjust these varying conditions, macrophages cDCs acquire spatiotemporal adaptations (STAs) at different stages of life cycle determine respond infection. The STAs acquired in response previous infections can result increased responsiveness infection, termed training, or reduced responses, paralysis, which extreme cases cause immunosuppression. Understanding developmental stage location where STAs, molecular cellular players involved induction, may afford opportunities harness beneficial outcomes avoid reverse deleterious effects. Here we review our current understanding macrophage cDC development, cycle, function, STA acquisition before, during, after infection.We propose a unified framework explain two cell types activities changing conditions space time coordinate immunosurveillance

Language: Английский

---

Monocytes and macrophages: emerging mechanisms and novel therapeutic targets in pulmonary fibrosis

AJP Cell Physiology, Journal Year: 2023, Volume and Issue: 325(4), P. C1046 - C1057

Published: Sept. 11, 2023

Pulmonary fibrosis results from a plethora of abnormal pathogenetic events. In idiopathic pulmonary (IPF), inhalational, environmental, or occupational exposures in genetically and epigenetically predisposed individuals trigger recurrent cycles alveolar epithelial cell injury, activation coagulation pathways, chemoattraction, differentiation monocytes into monocyte-derived macrophages (Mo-AMs). When these events happen intermittently repeatedly throughout the individual's life cycle, wound repair process becomes aberrant leading to bronchiolization distal air spaces, fibroblast accumulation, extracellular matrix deposition, loss alveolar-capillary architecture. The role immune dysregulation IPF pathogenesis progression has been underscored past mainly after disappointing immunosuppressant use patients; however, recent reports highlighting prognostic mechanistic roles Mo-AMs revived interest IPF. this review, we will discuss cells onset IPF, as well potential targeted therapies.

Language: Английский

---