ArticleThe Journal of biological chemistry2016
FcγRIIIa-Syk Co-signal Modulates CD4+ T-cell Response and Up-regulates Toll-like Receptor (TLR) Expression.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Increased levels of a pro-inflammatory IgG receptor in the midbrain of people with schizophrenia.Journal of neuroinflammation · 2022Article
- Complement System and Alarmin HMGB1 Crosstalk: For Better or Worse.Frontiers in immunology · 2022Review
- Blockade of TLR2 and TLR4 Attenuates Inflammatory Response and Parasite Load in Cutaneous Leishmaniasis.Frontiers in immunology · 2021Article
- A Two-Step Process of Effector Programming Governs CD4Cell reports · 2020Article
- Inhibition of SYK kinase does not confer a pro-proliferative or pro-invasive phenotype in breast epithelium or breast cancer cells.Oncotarget · 2020Article
- The role of Syk in peripheral T cells.Clinical immunology (Orlando, Fla.) · 2018Article
- Role of a non-canonical splice variant of theOncology letters · 2018Article
- SYK-targeted dendritic cell-mediated cytotoxic T lymphocytes enhance the effect of immunotherapy on retinoblastoma.Journal of cancer research and clinical oncology · 2018Article
- CD32 Ligation Promotes the Activation of CD4Frontiers in immunology · 2018Article
- FcγRIIIa Signaling Modulates Endosomal TLR Responses in Human CD4Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Editorial: Immune Complexes in Disease Pathology.Frontiers in immunology · 2017Article
- T cells in Systemic Lupus Erythematosus.Current opinion in immunology · 2016Review
- Human CD4(+) T-Cells: A Role for Low-Affinity Fc Receptors.Frontiers in immunology · 2016Review
- HMGB1 May Be a Biomarker for Predicting the Outcome in Patients with Polymyositis /Dermatomyositis with Interstitial Lung Disease.PloS one · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
CD4(+) T-cells in systemic lupus erythematosus (SLE) patients show altered T-cell receptor signaling, which utilizes Fc-receptor γ-chain FcRγ-Syk. A role for FcγRIIIa activation from immune complex (IC) ligation and sublytic terminal complement complex (C5b-9) in CD4(+) T-cell responses is not investigated. In this study, we show that the ICs present in SLE patients by ligating to FcγRIIIa on CD4(+) T-cells phosphorylate Syk and provide a co-stimulatory signal to CD4(+) T-cells in the absence of CD28 signal. This led to the development of pathogenic IL-17A(+) and IFN-γ(high) CD4(+) T-cells in vitro. Cytokines IL-1β, IL-6, TGF-β1, and IL-23 were the only requirement for the development of both populations. SLE patients CD4(+) T-cells that expressed CD25, CD69, and CD98 bound to ICs showed pSyk and produced IFN-γ and IL-17A. This FcγRIIIa-mediated co-signal differentially up-regulated the expression of IFN pathway genes compared with CD28 co-signal. FcγRIIIa-pSyk up-regulated several toll-like receptor genes as well as the HMGB1 and MyD88 gene transcripts. ICs co-localized with these toll-like receptor pathway proteins. These results suggest a role for the FcγRIIIa-pSyk signal in modulating adaptive immune responses.
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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.