Mer receptor tyrosine kinase (MerTK) plays a central role in mediating the non-inflammatory clearance of apoptotic cells. Impairment of MerTK causes an excess of apoptotic cells, favouring a loss of immune tolerance towards nuclear and inner membrane antigens and the development of autoimmunity. Upregulation of MerTK in myeloid cells is a critical checkpoint for resolution of inflammation and maintenance of tissue homeostasis. Synovial expansion of MerTK-positive macrophage subsets has been recently associated with stable remission in rheumatoid arthritis. However, induction of MerTK may also initiate an aberrant post-inflammatory reparative fibrosis, as shown in some fibrosing diseases, such as idiopathic pulmonary fibrosis, post-ischemic myocardial fibrosis, NASH-derived liver cirrhosis, and IgG4-related disease.
Growing evidence supports an active role of MerTK in inducing the release of anti-inflammatory mediators (eg, IL-10, resolvins) and profibrotic molecules (eg, osteopontin/SPP-1, TGFbeta). In this Research Topic, we would like to delve into the molecular and cellular pathways through which MerTK shuts down inflammation and triggers post-inflammatory fibrosis. Additionally, we aim to investigate the potential role of MerTK in further inflammatory and fibrotic disorders.
This research topic mainly welcomes contributions of Original research. Opinion pieces containing insightful Viewpoints and original Perspectives may also be considered. We welcome submissions based on (but not limited to) the following topics:
- the expression and activity of MerTK in inflammatory and fibrosing diseases;
- the phenotypes of cells expressing MerTK and its ligands in pathological conditions;
- the pathways and mediators involved in MerTK induction and function;
- the effects of MerTK stimulation and/or inhibition ex vivo or in animal models of inflammatory and fibrosing diseases;
- the immunological aspects linked to MerTK-mediated fibrogenesis.
Mer receptor tyrosine kinase (MerTK) plays a central role in mediating the non-inflammatory clearance of apoptotic cells. Impairment of MerTK causes an excess of apoptotic cells, favouring a loss of immune tolerance towards nuclear and inner membrane antigens and the development of autoimmunity. Upregulation of MerTK in myeloid cells is a critical checkpoint for resolution of inflammation and maintenance of tissue homeostasis. Synovial expansion of MerTK-positive macrophage subsets has been recently associated with stable remission in rheumatoid arthritis. However, induction of MerTK may also initiate an aberrant post-inflammatory reparative fibrosis, as shown in some fibrosing diseases, such as idiopathic pulmonary fibrosis, post-ischemic myocardial fibrosis, NASH-derived liver cirrhosis, and IgG4-related disease.
Growing evidence supports an active role of MerTK in inducing the release of anti-inflammatory mediators (eg, IL-10, resolvins) and profibrotic molecules (eg, osteopontin/SPP-1, TGFbeta). In this Research Topic, we would like to delve into the molecular and cellular pathways through which MerTK shuts down inflammation and triggers post-inflammatory fibrosis. Additionally, we aim to investigate the potential role of MerTK in further inflammatory and fibrotic disorders.
This research topic mainly welcomes contributions of Original research. Opinion pieces containing insightful Viewpoints and original Perspectives may also be considered. We welcome submissions based on (but not limited to) the following topics:
- the expression and activity of MerTK in inflammatory and fibrosing diseases;
- the phenotypes of cells expressing MerTK and its ligands in pathological conditions;
- the pathways and mediators involved in MerTK induction and function;
- the effects of MerTK stimulation and/or inhibition ex vivo or in animal models of inflammatory and fibrosing diseases;
- the immunological aspects linked to MerTK-mediated fibrogenesis.