Expression of intracellular transforming growth factor-betal in CD4 +CD25+ cells in patients with systemic lupus erythematosus

Ling Ying Lu, Jiung Jun Chu, Pei-Jung Lu, Ping Kuang Sung, Chei Mei Hsu, Jui Cheng Tseng

Research output: Contribution to journalArticle

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Abstract

Background and Purpose: The CD4+CD25+ regulatory T (Treg) cells exert immunoregulatory functions in various autoimmune diseases, in part through transforming growth factor-beta1 (TGF-β1), and can be expanded by TGF-β1 stimulation in normal subjects. This study aimed to examine intrinsic TGF-β1 expression and the response to TGF-β1 stimulation of this CD4+CD25+ subset in patients with systemic lupus erythematosus (SLE). Methods: Flow cytometry with multicolor staining of CD4+, CD25+, and TGF-β1 was used to quantify the percentage of CD4+CD25+ T cells in fresh peripheral blood and TGF-β1-stimulated peripheral blood mononuclear cell (PBMC) cultures, and their corresponding intracellular TGF-β1 expression. Results: In fresh peripheral blood, we found that decreased percentages of CD4+CD25+/CD4+ in SLE patients were associated with disease activity and renal involvement. Intracellular TGF-β1 expression of CD4+CD25+ cells was significantly elevated in SLE compared with matched controls (p<0.001). In addition, there was significant negative correlation between TGF-β1 expression and percentage of CD4+CD25+ cells present (r = -0.432, p=0.004). Nevertheless, in ex vivo unstimulated PBMC cultures, the percentage and intracellular TGF-β1 expression of CD4+CD25+ cells of SLE were normalized to the levels of the control group. In TGF-β1- stimulated PBMC cultures, CD4+CD25+ cells and their intracellular TGF-β1 expression were significantly increased (p<0.001), both in SLE and controls. Moreover, the increments in the percentage of CD4 +CD25+ cells and intracellular TGF-β1 expression by TGF-β1 stimulation were comparable in SLE and controls, and were not significantly influenced by disease activity or renal involvement in SLE. Conclusions: CD4+CD25+ cells were deficient in peripheral blood but not impaired either in intrinsic TGF-β1 expression or in response to TGF-β1 stimulation in patients with SLE. This study suggests that TGF-β1, by inducing CD4+CD25+ cells, has potential clinical application in treating SLE.

Original languageEnglish
Pages (from-to)165-173
Number of pages9
JournalJournal of Microbiology, Immunology and Infection
Volume41
Issue number2
Publication statusPublished - 2008 Apr 1

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Transforming Growth Factor beta1
Transforming Growth Factors
Systemic Lupus Erythematosus
Blood Cells
Cell Culture Techniques
Regulatory T-Lymphocytes
Kidney

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology and Microbiology(all)
  • Microbiology (medical)
  • Infectious Diseases

Cite this

Lu, Ling Ying ; Chu, Jiung Jun ; Lu, Pei-Jung ; Sung, Ping Kuang ; Hsu, Chei Mei ; Tseng, Jui Cheng. / Expression of intracellular transforming growth factor-betal in CD4 +CD25+ cells in patients with systemic lupus erythematosus. In: Journal of Microbiology, Immunology and Infection. 2008 ; Vol. 41, No. 2. pp. 165-173.
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abstract = "Background and Purpose: The CD4+CD25+ regulatory T (Treg) cells exert immunoregulatory functions in various autoimmune diseases, in part through transforming growth factor-beta1 (TGF-β1), and can be expanded by TGF-β1 stimulation in normal subjects. This study aimed to examine intrinsic TGF-β1 expression and the response to TGF-β1 stimulation of this CD4+CD25+ subset in patients with systemic lupus erythematosus (SLE). Methods: Flow cytometry with multicolor staining of CD4+, CD25+, and TGF-β1 was used to quantify the percentage of CD4+CD25+ T cells in fresh peripheral blood and TGF-β1-stimulated peripheral blood mononuclear cell (PBMC) cultures, and their corresponding intracellular TGF-β1 expression. Results: In fresh peripheral blood, we found that decreased percentages of CD4+CD25+/CD4+ in SLE patients were associated with disease activity and renal involvement. Intracellular TGF-β1 expression of CD4+CD25+ cells was significantly elevated in SLE compared with matched controls (p<0.001). In addition, there was significant negative correlation between TGF-β1 expression and percentage of CD4+CD25+ cells present (r = -0.432, p=0.004). Nevertheless, in ex vivo unstimulated PBMC cultures, the percentage and intracellular TGF-β1 expression of CD4+CD25+ cells of SLE were normalized to the levels of the control group. In TGF-β1- stimulated PBMC cultures, CD4+CD25+ cells and their intracellular TGF-β1 expression were significantly increased (p<0.001), both in SLE and controls. Moreover, the increments in the percentage of CD4 +CD25+ cells and intracellular TGF-β1 expression by TGF-β1 stimulation were comparable in SLE and controls, and were not significantly influenced by disease activity or renal involvement in SLE. Conclusions: CD4+CD25+ cells were deficient in peripheral blood but not impaired either in intrinsic TGF-β1 expression or in response to TGF-β1 stimulation in patients with SLE. This study suggests that TGF-β1, by inducing CD4+CD25+ cells, has potential clinical application in treating SLE.",
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Expression of intracellular transforming growth factor-betal in CD4 +CD25+ cells in patients with systemic lupus erythematosus. / Lu, Ling Ying; Chu, Jiung Jun; Lu, Pei-Jung; Sung, Ping Kuang; Hsu, Chei Mei; Tseng, Jui Cheng.

In: Journal of Microbiology, Immunology and Infection, Vol. 41, No. 2, 01.04.2008, p. 165-173.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Expression of intracellular transforming growth factor-betal in CD4 +CD25+ cells in patients with systemic lupus erythematosus

AU - Lu, Ling Ying

AU - Chu, Jiung Jun

AU - Lu, Pei-Jung

AU - Sung, Ping Kuang

AU - Hsu, Chei Mei

AU - Tseng, Jui Cheng

PY - 2008/4/1

Y1 - 2008/4/1

N2 - Background and Purpose: The CD4+CD25+ regulatory T (Treg) cells exert immunoregulatory functions in various autoimmune diseases, in part through transforming growth factor-beta1 (TGF-β1), and can be expanded by TGF-β1 stimulation in normal subjects. This study aimed to examine intrinsic TGF-β1 expression and the response to TGF-β1 stimulation of this CD4+CD25+ subset in patients with systemic lupus erythematosus (SLE). Methods: Flow cytometry with multicolor staining of CD4+, CD25+, and TGF-β1 was used to quantify the percentage of CD4+CD25+ T cells in fresh peripheral blood and TGF-β1-stimulated peripheral blood mononuclear cell (PBMC) cultures, and their corresponding intracellular TGF-β1 expression. Results: In fresh peripheral blood, we found that decreased percentages of CD4+CD25+/CD4+ in SLE patients were associated with disease activity and renal involvement. Intracellular TGF-β1 expression of CD4+CD25+ cells was significantly elevated in SLE compared with matched controls (p<0.001). In addition, there was significant negative correlation between TGF-β1 expression and percentage of CD4+CD25+ cells present (r = -0.432, p=0.004). Nevertheless, in ex vivo unstimulated PBMC cultures, the percentage and intracellular TGF-β1 expression of CD4+CD25+ cells of SLE were normalized to the levels of the control group. In TGF-β1- stimulated PBMC cultures, CD4+CD25+ cells and their intracellular TGF-β1 expression were significantly increased (p<0.001), both in SLE and controls. Moreover, the increments in the percentage of CD4 +CD25+ cells and intracellular TGF-β1 expression by TGF-β1 stimulation were comparable in SLE and controls, and were not significantly influenced by disease activity or renal involvement in SLE. Conclusions: CD4+CD25+ cells were deficient in peripheral blood but not impaired either in intrinsic TGF-β1 expression or in response to TGF-β1 stimulation in patients with SLE. This study suggests that TGF-β1, by inducing CD4+CD25+ cells, has potential clinical application in treating SLE.

AB - Background and Purpose: The CD4+CD25+ regulatory T (Treg) cells exert immunoregulatory functions in various autoimmune diseases, in part through transforming growth factor-beta1 (TGF-β1), and can be expanded by TGF-β1 stimulation in normal subjects. This study aimed to examine intrinsic TGF-β1 expression and the response to TGF-β1 stimulation of this CD4+CD25+ subset in patients with systemic lupus erythematosus (SLE). Methods: Flow cytometry with multicolor staining of CD4+, CD25+, and TGF-β1 was used to quantify the percentage of CD4+CD25+ T cells in fresh peripheral blood and TGF-β1-stimulated peripheral blood mononuclear cell (PBMC) cultures, and their corresponding intracellular TGF-β1 expression. Results: In fresh peripheral blood, we found that decreased percentages of CD4+CD25+/CD4+ in SLE patients were associated with disease activity and renal involvement. Intracellular TGF-β1 expression of CD4+CD25+ cells was significantly elevated in SLE compared with matched controls (p<0.001). In addition, there was significant negative correlation between TGF-β1 expression and percentage of CD4+CD25+ cells present (r = -0.432, p=0.004). Nevertheless, in ex vivo unstimulated PBMC cultures, the percentage and intracellular TGF-β1 expression of CD4+CD25+ cells of SLE were normalized to the levels of the control group. In TGF-β1- stimulated PBMC cultures, CD4+CD25+ cells and their intracellular TGF-β1 expression were significantly increased (p<0.001), both in SLE and controls. Moreover, the increments in the percentage of CD4 +CD25+ cells and intracellular TGF-β1 expression by TGF-β1 stimulation were comparable in SLE and controls, and were not significantly influenced by disease activity or renal involvement in SLE. Conclusions: CD4+CD25+ cells were deficient in peripheral blood but not impaired either in intrinsic TGF-β1 expression or in response to TGF-β1 stimulation in patients with SLE. This study suggests that TGF-β1, by inducing CD4+CD25+ cells, has potential clinical application in treating SLE.

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