ArticleAutoimmunity2009
The receptor tyrosine kinase MerTK regulates dendritic cell production of BAFF.
Article in Autoimmunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Anti-Axl antibody treatment reduces the severity of experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2020Article
- The role of TAM family receptors and ligands in the nervous system: From development to pathobiology.Pharmacology & therapeutics · 2018Review
- Mechanism of Mer receptor tyrosine kinase inhibition of glomerular endothelial cell inflammation.Journal of leukocyte biology · 2018Article
- Protease-Activated Receptor 1 Enhances Poly I:C Induction of the Antiviral Response in Macrophages and Mice.Journal of innate immunity · 2017Article
- A benzenediamine derivate FC-99 attenuates lupus nephritis in MRL/lpr mice via inhibiting myeloid dendritic cell-secreted BAFF.Acta biochimica et biophysica Sinica · 2016Article
- MERTK as negative regulator of human T cell activation.Journal of leukocyte biology · 2015Article
- The Mertk receptor tyrosine kinase promotes T-B interaction stimulated by IgD B-cell receptor cross-linking.Journal of autoimmunity · 2014Article
- Molecular control of steady-state dendritic cell maturation and immune homeostasis.Annual review of immunology · 2013Review
- Article
- Impaired apoptotic cell clearance in the germinal center by Mer-deficient tingible body macrophages leads to enhanced antibody-forming cell and germinal center responses.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Increased hematopoietic cells in the mertk-/- mouse peritoneal cavity: a result of augmented migration.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The MerTK receptor tyrosine kinase is an important negative regulator of dendritic cell function and is required to prevent B cell autoimmunity in vivo. It is not currently known however, if any causal relationship exists between these two aspects of MerTK function. We sought to determine if dendritic cells (DC) from mice lacking MerTK (mertk(- / - ) mice) have characteristics that may aid in the development of B cell autoimmunity. Specifically, we found that mertk(- / - ) mice contain an elevated number of splenic DC, and this population contains an elevated proportion of cells secreting the critical B cell pro-survival factor, B cell activating factor (BAFF). Elevated numbers of BAFF-secreting cells were also detected among mertk(- / - ) bone marrow-derived dendritic cell (BMDC) populations. This was observed in both resting BMDC, and BMDC stimulated with lipopolysaccharide (LPS) or treated with exogenous apoptotic cells. We also found that DC in general have a pro-survival effect on resting B cells in co-culture. However, despite containing more BAFF-secreting cells, mertk(- / - ) BMDC were not superior to C57BL/6 or baff-deficient BMDC at promoting B cell survival. Furthermore, using decoy receptors, we show that DC may promote B cell survival and autoimmunity through a BAFF-and a proliferation-inducing ligand-independent mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.