ReviewCurrent opinion in rheumatology2010
Implications of the parent-into-F1 model for human lupus pathogenesis: roles for cytotoxic T lymphocytes and viral pathogens.
Review in Current opinion in rheumatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- B cell depletion in murine lupus using cytotoxic T lymphocytes in vivo: Feasibility and benefit.Cellular immunology · 2020Article
- Both perforin and FasL are required for optimal CD8 T cell control of autoreactive B cells and autoantibody production in parent-into-F1 lupus mice.Clinical immunology (Orlando, Fla.) · 2018Article
- Intrinsic Differences in Donor CD4 T Cell IL-2 Production Influence Severity of Parent-into-F1 Murine Lupus by Skewing the Immune Response Either toward Help for B Cells and a Sustained Autoantibody Response or toward Help for CD8 T Cells and a Downregulatory Th1 Response.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Lupus and Epstein-Barr.Current opinion in rheumatology · 2012Review
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
purpose of reviewThe central role of CD4 T cells in lupus pathogenesis is well recognized; however, the mechanism by which CD4 T cells lose tolerance and promote humoral autoimmunity remains unclear. This review examines mechanisms elucidated in the parent-into-F1 model of lupus and their possible parallels in human lupus pathogenesis. RECENT
findingsIn the parent-into-F1 model, lupus results from the transfer of normal, foreign reactive CD4 T cells targeted to intrinsically normal F1 B cells. Transfer of normal CD8 T cells prevents lupus, whereas transfer of CD8 T cells with killing defects does not but is correctable with additional in-vivo enhancement of CD8 cytotoxic T lymphocyte (CTL) function. The parent-into-F1 model has two major similarities to Epstein-Barr virus infection: CD4 T-cell-driven polyclonal B-cell hyperactivity and a critical dependence on CD8 CTL for elimination of activated B cells. These similarities are discussed in relation to human lupus pathogenesis. SUMMARY: Work in the parent-into-F1 model supports the idea that lupus may result from defective CD8 T-cell function and that therapeutic enhancement of CD8 effectors with selective targeting to autoreactive B cells may be beneficial. Despite strong evidence linking Epstein-Barr virus infection with human lupus, the exact nature of this link requires further study.
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