ArticleJournal of clinical immunology2011
Resistance to exogenous TGF-β effects in patients with systemic lupus erythematosus.
Article in Journal of clinical immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Th1-related transcription factors and cytokines in systemic lupus erythematosus.Frontiers in immunology · 2023Review
- Tofacitinib Ameliorates Lupus Through Suppression of T Cell Activation Mediated by TGF-Beta Type I Receptor.Frontiers in immunology · 2021Article
- Reevaluation of Pluripotent Cytokine TGF-β3 in Immunity.International journal of molecular sciences · 2018Review
- Aberrant T Cell Signaling and Subsets in Systemic Lupus Erythematosus.Frontiers in immunology · 2018Review
- Therapeutic potential of regulatory cytokines that target B cells.International immunology · 2016Review
- PD-1 induction through TCR activation is partially regulated by endogenous TGF-β.Cellular & molecular immunology · 2015Article
- Roles of pro- and anti-inflammatory cytokines in the pathogenesis of SLE.Journal of biomedicine & biotechnology · 2012Review
- The problem of accelerated atherosclerosis in systemic lupus erythematosus: insights into a complex co-morbidity.Thrombosis and haemostasis · 2011Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mechanisms underlying the loss of self-tolerance in systemic lupus erythematosus (SLE) are incompletely deciphered. TGF-β plays a key role in self-tolerance demonstrated by the onset of a fatal autoimmune syndrome associated with lupus autoantibodies in mice lacking a functional TGF-β receptor. The present work aims to define whether resistance to TGF-β might contribute to the pathogenesis of SLE.
methodsTwenty-two patients with active SLE, 16 with other connective tissue diseases, and 10 healthy controls were prospectively included in this study. The effects of exogenous TGF-β1 on IL-2-dependent T-cell proliferation, IFN-γ secretion, and target gene transcription were analyzed on peripheral blood mononuclear cells.
resultsOur results showed that 75% of patients with SLE or other connective tissue diseases were totally or partially resistant to the effects of TGF-β1. The responses to the anti-proliferative and transcriptional effects of TGF-β were, however, discordant in a high proportion of our patients. Hence, we distinguish three distinct profiles of resistance to TGF-β1 and suggest that patients may exhibit different defects affecting distinct points of TGF-β1 signaling pathways.
conclusionOur data demonstrate the presence of an impaired response of peripheral cells to TGF-β1 in patients with active SLE that may participate to the pathogenesis of the disease. Further studies will be necessary to delineate the mechanisms underlying the lymphocyte resistance to TGF-β1 in SLE.
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