Nature of IgG anti-lymphocyte autoantibody-reactive molecules shed from activated T cells in systemic lupus erythematosus

1988 ◽  
Vol 8 (4) ◽  
pp. 165-170 ◽  
Author(s):  
S. Minota ◽  
J. B. Winfield
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Activated T Cells

scholarly journals Altered Cell Surface N-Glycosylation of Resting and Activated T Cells in Systemic Lupus Erythematosus

2019 ◽  
Vol 20 (18) ◽  
pp. 4455 ◽  
Author(s):  
Enikő Szabó ◽  
Ákos Hornung ◽  
Éva Monostori ◽  
Márta Bocskai ◽  
Ágnes Czibula ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
T Cell ◽  
Cell Surface ◽  
Lupus Erythematosus ◽  
Lectin Binding ◽  
Systemic Lupus ◽  
Activated T Cells ◽  
Neuraminidase Treatment ◽  
Altered Cell

Altered cell surface glycosylation in congenital and acquired diseases has been shown to affect cell differentiation and cellular responses to external signals. Hence, it may have an important role in immune regulation; however, T cell surface glycosylation has not been studied in systemic lupus erythematosus (SLE), a prototype of autoimmune diseases. Analysis of the glycosylation of T cells from patients suffering from SLE was performed by lectin-binding assay, flow cytometry, and quantitative real-time PCR. The results showed that resting SLE T cells presented an activated-like phenotype in terms of their glycosylation pattern. Additionally, activated SLE T cells bound significantly less galectin-1 (Gal-1), an important immunoregulatory lectin, while other lectins bound similarly to the controls. Differential lectin binding, specifically Gal-1, to SLE T cells was explained by the increased gene expression ratio of sialyltransferases and neuraminidase 1 (NEU1), particularly by elevated ST6 beta-galactosamide alpha-2,6-sialyltranferase 1 (ST6GAL1)/NEU1 and ST3 beta-galactoside alpha-2,3-sialyltransferase 6 (ST3GAL6)/NEU1 ratios. These findings indicated an increased terminal sialylation. Indeed, neuraminidase treatment of cells resulted in the increase of Gal-1 binding. Altered T cell surface glycosylation may predispose the cells to resistance to the immunoregulatory effects of Gal-1, and may thus contribute to the pathomechanism of SLE.

Subsets of Activated T Cells in Patients with Systemic Lupus Erythematosus: the Relation to Cell Cycle

1997 ◽  
Vol 26 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Y. Tokano ◽  
S. Morimoto ◽  
T. Hishikawa ◽  
A. Murashima ◽  
M. Abe ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Cycle ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Activated T Cells

scholarly journals Umbilical Cord-Derived Mesenchymal Stem Cells Suppress Autophagy of T Cells in Patients with Systemic Lupus Erythematosus via Transfer of Mitochondria

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Jinyun Chen ◽  
Qian Wang ◽  
Xuebing Feng ◽  
Zhuoya Zhang ◽  
Linyu Geng ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Stem Cells ◽  
T Cells ◽  
T Cell ◽  
Lupus Erythematosus ◽  
Cell Apoptosis ◽  
Systemic Lupus ◽  
Activated T Cells ◽  
T Cell Apoptosis ◽  
Autophagic Activity

Aberrant autophagy played an important role in the pathogenesis of autoimmune diseases, especially in systemic lupus erythematosus (SLE). In this study, we showed that T cells from SLE patients had higher autophagic activity than that from healthy controls. A correlation between autophagic activity and apoptotic rate was observed in activated T cells. Moreover, activation of autophagy with rapamycin increased T cell apoptosis, whereas inhibition of autophagy with 3-MA decreased T cell apoptosis. Umbilical cord-derived mesenchymal stem cells (UC-MSCs) could inhibit respiratory mitochondrial biogenesis in activated T cells to downregulate autophagy and consequently decrease T cell apoptosis through mitochondrial transfer and thus may play an important role in SLE treatment.

scholarly journals The Progress of Investigating the CD137-CD137L Axis as a Potential Target for Systemic Lupus Erythematosus

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1044 ◽  
Author(s):  
Anselm Mak ◽  
Herbert Schwarz
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Critical Role ◽  
Costimulatory Molecules ◽  
Tumour Necrosis Factor Receptor ◽  
Systemic Lupus ◽  
Activated T Cells ◽  
Autoantibody Production ◽  
Proinflammatory Responses

Costimulatory molecules facilitate cross-talks among leukocytes via mutual stimulatory and inhibitory signalling, contributing to diverse immunological outcomes in normal physiological responses and pathological conditions. Systemic lupus erythematosus (SLE) is a complex multi-systemic autoimmune condition in which cellular communication through the involvement of costimulatory molecules is crucial in driving proinflammatory responses from the stage of autoantigen presentation to the subsequent process of pathogenic autoantibody production. While the physiology of the costimulatory systems including OX40-OX40L, CD28/CTLA-4-CD80/86, ICOS-B7RP1 and CD70-CD27 has been relatively well studied in SLE, recent data on the immunopathology of the CD137-CD137 ligand (CD137L) system in murine lupus models and patients with SLE highlight the critical role of this costimulatory system in initiating and perpetuating the diverse clinical and serological phenotypes of SLE. CD137, a membrane-bound receptor which belongs to the tumour necrosis factor receptor superfamily, is mainly expressed on activated T cells. Activation of the CD137 receptor via its interaction with CD137L which is expressed on antigen present cells (APC) including B cells, triggers bi-directional signalling; that is, signalling through CD137 as well as signalling through CD137L (reverse signalling), which further activates T cells and polarizes them to the Th1/Tc1 pathway. Further, via reverse CD137L signalling it enhances differentiation and maturation of the APC, particularly of dendritic cells, which subsequently drive proinflammatory cytokine production. In this review, recent data including our experience in the manipulation of CD137L signalling pertaining to the pathophysiology of SLE will be critically reviewed. More in-depth understanding of the biology of the CD137-CD137L co-stimulation system opens an opportunity to identify new prognostic biomarkers and the design of novel therapeutic approaches for advancing the management of SLE.

Increased Expression of Functional Fas-Ligand in Activated T Cells from Patients with Systemic Lupus Erythematosus

Autoimmunity ◽  
1997 ◽  
Vol 25 (4) ◽  
pp. 213-221 ◽  
Author(s):  
Birgit Kovacs ◽  
Stamatis-Nick C. Liossis ◽  
Gregory J. Dennis ◽  
George C. Tsokos
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Fas Ligand ◽  
Systemic Lupus ◽  
Activated T Cells

The Systemic Activation of Programmed Death 1-PD-L1 Axis Protects Systemic Lupus Erythematosus Model from Nephritis

2017 ◽  
Vol 46 (5) ◽  
pp. 371-379 ◽  
Author(s):  
Wenjun Liao ◽  
Hua Zheng ◽  
Sha Wu ◽  
Yanmei Zhang ◽  
Wei Wang ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
B Cells ◽  
Lupus Erythematosus ◽  
Enzyme Linked Immunosorbent Assay ◽  
Systemic Lupus ◽  
Activated T Cells ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Ifn Γ

Background: Systemic lupus erythematosus (SLE) is characterized by abnormal activated T cells, autoreactive B cells, and massive cytokines. The CD4+ T cells determined B-cells differentiation and cytokines production. The programmed death 1 (PD-1) is the checkpoint immunoinhibitory receptor of activated T cells, and its engagement could exhaust T cells. In this study, we investigated the role of PD-1 systemic engagement with PD-L1-Ig in lupus-like nephritis in SLE mice. Methods: The murine PD-L1-Ig was injected into SLE-prone mice. The proteinuria and survival ratio were monitored. The production of anti-dsDNA autoantibodies and cytokines in serum were measured by enzyme-linked immunosorbent assay. The cytokine-producing T cells (interferon-γ, IFN-γ and IL-17α) in kidney and spleen were detected with flowcytometry. The pathological evaluation of the Ig deposition in the glomeruliand was determined with immunofluorescence. Lymphocytes in 24-h urine were detected with flowcytometry. Results: The systemic administration of PD-L1-Ig activated PD-1-PD-L1 axis of CD4+ T lymphocytes, suppressed Th17 formation in many organs, including the spleen and the kidney, demolished abnormal production of cytokines (IFN-γ, IL-17, and IL-10) and anti-dsDNA autoantibodies in serum, inhibited immunoglobulin G deposition in the glomeruli with the decrease of proteinuria, and activated T cells in urine. Accordingly, the systemic conjugation of PD-L1-PD-1 impaired renal autoimmune injure and prolonged survival time. Conclusion: Our research demonstrated that the protective function of systemic activation of PD-1-PD-L1 axis with PD-L1-Ig attenuates the nephritis in SLE-prone mice, which facilitates us to understand the suppressive function of PD-1-PD-L1 axis in the pathogenesis and progress of the lupus nephritis, and to explore a possible effective therapeutic strategy to SLE.

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