ArticleArthritis and rheumatism2012
Requirement of myeloid cell-specific Fas expression for prevention of systemic autoimmunity in mice.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Comprehensive analysis of myeloid reporter mice.bioRxiv : the preprint server for biology · 2025Article
- A novel combination approach to effectively reduce inflammation and neurodegeneration in multiple sclerosis models.Neurochemistry international · 2024Article
- A Novel Microglia-Specific Transcriptional Signature Correlates With Behavioral Deficits in Neuropsychiatric Lupus.Frontiers in immunology · 2020Article
- Remarkably Robust Antiviral Immune Response despite Combined Deficiency in Caspase-8 and RIPK3.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Bim suppresses the development of SLE by limiting myeloid inflammatory responses.The Journal of experimental medicine · 2017Article
- The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- The caspase-8/RIPK3 signaling axis in antigen presenting cells controls the inflammatory arthritic response.Arthritis research & therapy · 2017Article
- The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases.Nature reviews. Rheumatology · 2016Review
- How Mouse Macrophages Sense What Is Going On.Frontiers in immunology · 2016Review
- Conditional deletion of caspase-8 in macrophages alters macrophage activation in a RIPK-dependent manner.Arthritis research & therapy · 2015Article
- The Interplay Between Monocytes/Macrophages and CD4(+) T Cell Subsets in Rheumatoid Arthritis.Frontiers in immunology · 2015Review
- Caspase-8 acts as a molecular rheostat to limit RIPK1- and MyD88-mediated dendritic cell activation.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Fas signaling in macrophages promotes chronicity in K/BxN serum-induced arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Somatic mutagenesis in autoimmunity.Autoimmunity · 2013Review
- Managing macrophages in rheumatoid arthritis by reform or removal.Current rheumatology reports · 2012Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveThe death receptor Fas is a critical mediator of the extrinsic apoptotic pathway, and its role in mediating lymphoproliferation has been extensively examined. The present study was undertaken to investigate the impact of myeloid cell-specific loss of Fas.
methodsMice with Fas flanked by loxP sites (Fas(flox/flox) ) were crossed with mice expressing Cre under control of the murine lysozyme M gene promoter (Cre(LysM) ), which functions in mature lysozyme-expressing cells of the myelomonocytic lineage. The genotype for Cre(LysM) Fas(flox/flox) mice was verified by polymerase chain reaction and flow cytometric analysis. Flow cytometric analysis was also used to characterize myeloid, dendritic, and lymphoid cell distribution and activation in bone marrow, blood, and spleen. Luminex-based assays and enzyme-linked immunosorbent assays were used to measure serum cytokine/chemokine and immunoglobulin levels. Renal damage or dysfunction was examined by immunohistochemical and immunofluorescence analysis.
resultsCre(LysM) Fas(flox/flox) mice exhibited a systemic lupus erythematosus (SLE)-like disease that included leukocytosis, splenomegaly, hypergammaglobulinemia, antinuclear autoantibody and proinflammatory cytokine production, and glomerulonephritis. Loss of Fas in myeloid cells increased levels of both Gr-1(low) and Gr-1(intermediate) blood monocytes and splenic macrophages and, in a paracrine manner, incited activation of conventional dendritic cells and lymphocytes in Cre(LysM) Fas(flox/flox) mice.
conclusionTaken together, these results suggest that loss of Fas in myeloid cells is sufficient to induce inflammatory phenotypes in mice, reminiscent of an SLE-like disease. Thus, Fas in myeloid cells may be considered a suppressor of systemic autoimmunity.
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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.