The abnormal apoptosis of T cell subsets and possible involvement of IL-10 in systemic lupus erythematosus

Wang, Huijuan; Xu, Juan; Ji, Xiaohui; Yang, Xiaofan; Sun, Kai; Liu, Xiaohua; Shen, Ya

doi:10.1016/j.cellimm.2005.08.031

Cited by 36 publications

(35 citation statements)

References 16 publications

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“…[23][24][25] Recent studies indicate that regulatory cells exert their function by the production of antiinflammatory cytokines such as IL-10, 26,27 which in turn may exert its antiinflammatory action by inducing lymphocyte apoptosis. 28 In this sense, we have also demonstrated that in the group of steroid-responsive patients, in whom increased Tand B-cell apoptosis was observed, there was a strong relationship between good outcome and high expression of mucosal IL-10. Elevation of IL-10 both at baseline and after treatment argues in favor of a role for this cytokine in the adequate resolution of inflammatory process in response to therapy.…”

Section: Discussionmentioning

confidence: 75%

Apoptosis resistance of mucosal lymphocytes and IL-10 deficiency in patients with steroid-refractory Crohnʼs disease

Santaolalla¹,

Mañé²,

Pedrosa³

et al. 2011

Inflammatory Bowel Diseases

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Apoptosis resistance of mucosal T and B cells in steroid-refractory and -dependent CD patients appears during the evolution of the acute phase, limiting its clinical application as a predictor marker. In contrast, increased expression of IL-10 at an early stage of active steroid-sensitive CD patients supports its usefulness at predicting a good steroid response. Steroid-dependent and -refractory CD patients share similar molecular and cellular pathophysiological mechanisms.

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Section: Discussionmentioning

confidence: 75%

Apoptosis resistance of mucosal lymphocytes and IL-10 deficiency in patients with steroid-refractory Crohnʼs disease

Santaolalla¹,

Mañé²,

Pedrosa³

et al. 2011

Inflammatory Bowel Diseases

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“…The interleukin (IL)-10 signaling pathway was among other notable pathways found to be activated or, otherwise, altered in the SLE patients who were profiled. This is likely due to the abnormal apoptosis of T-cell subsets observed in SLE patients [21, 22]. …”

Section: Resultsmentioning

confidence: 99%

Development of Potential Pharmacodynamic and Diagnostic Markers for Anti-IFN-α Monoclonal Antibody Trials in Systemic Lupus Erythematosus

Yao¹,

Higgs²,

Morehouse³

et al. 2009

Human Genomics and Proteomics

116

158

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To identify potential pharmacodynamic biomarkers to guide dose selection in clinical trials using anti-interferon-alpha (IFN-α) monoclonal antibody (mAb) therapy for systemic lupus erythematosus (SLE), we used an Affymetrix human genome array platform and identified 110 IFN-α/β-inducible transcripts significantly upregulated in whole blood (WB) of 41 SLE patients. The overexpression of these genes was confirmed prospectively in 54 additional SLE patients and allowed for the categorization of the SLE patients into groups of high, moderate, and weak overexpressers of IFN-α/β-inducible genes. This approach could potentially allow for an accurate assessment of drug target neutralization in early trials of anti-IFN-α mAb therapy for SLE. Furthermore, ex vivo stimulation of healthy donor peripheral blood mononuclear cells with SLE patient serum and subsequent neutralization with anti-IFN-α mAb or anti-IFN-α receptor mAb showed that anti-IFN-α mAb has comparable effects of neutralizing the overexpression of type I IFN-inducible genes as that of anti-IFNAR mAb. These results suggest that IFN-α, and not other members of type I IFN family in SLE patients, is mainly responsible for the induction of type I IFN-inducible genes in WB of SLE patients. Taken together, these data strengthen the view of IFN-α as a therapeutic target for SLE.

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“…Given the heterogeneous nature of rheumatoid arthritis, and evidence for variation in the ratio of CD4 + /CD8 + T cells changes in autoimmune diseases such as Systemic Lupus Erythematosus (SLE) [26-28], we first characterized the composition of peripheral blood T cell subsets in RA patients using flow cytometry. Nonparametric unpaired student's T test was used to detect possible differences in the two T cell subsets between normal versus RA patients.…”

Section: Resultsmentioning

confidence: 99%

TRAIL Death Receptor-4, Decoy Receptor-1 and Decoy Receptor-2 Expression on CD8+ T Cells Correlate with the Disease Severity in Patients with Rheumatoid Arthritis

Bişgin

Terzıoğlu

Aydın

et al. 2010

BMC Musculoskelet Disord

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BackgroundRheumatoid Arthritis (RA) is a chronic autoimmune inflammatory disorder. Although the pathogenesis of disease is unclear, it is well known that T cells play a major role in both development and perpetuation of RA through activating macrophages and B cells. Since the lack of TNF-Related Apoptosis Inducing Ligand (TRAIL) expression resulted in defective thymocyte apoptosis leading to an autoimmune disease, we explored evidence for alterations in TRAIL/TRAIL receptor expression on peripheral T lymphocytes in the molecular mechanism of RA development.MethodsThe expression of TRAIL/TRAIL receptors on T cells in 20 RA patients and 12 control individuals were analyzed using flow cytometry. The correlation of TRAIL and its receptor expression profile was compared with clinical RA parameters (RA activity scored as per DAS28) using Spearman Rho Analysis.ResultsWhile no change was detected in the ratio of CD4+ to CD8+ T cells between controls and RA patient groups, upregulation of TRAIL and its receptors (both death and decoy) was detected on both CD4+ and CD8+ T cells in RA patients compared to control individuals. Death Receptor-4 (DR4) and the decoy receptors DcR1 and DcR2 on CD8+ T cells, but not on CD4+ T cells, were positively correlated with patients' DAS scores.ConclusionsOur data suggest that TRAIL/TRAIL receptor expression profiles on T cells might be important in revelation of RA pathogenesis.

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The abnormal apoptosis of T cell subsets and possible involvement of IL-10 in systemic lupus erythematosus

Cited by 36 publications

References 16 publications

Apoptosis resistance of mucosal lymphocytes and IL-10 deficiency in patients with steroid-refractory Crohnʼs disease

Apoptosis resistance of mucosal lymphocytes and IL-10 deficiency in patients with steroid-refractory Crohnʼs disease

Development of Potential Pharmacodynamic and Diagnostic Markers for Anti-IFN-α Monoclonal Antibody Trials in Systemic Lupus Erythematosus

TRAIL Death Receptor-4, Decoy Receptor-1 and Decoy Receptor-2 Expression on CD8+ T Cells Correlate with the Disease Severity in Patients with Rheumatoid Arthritis

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