Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells (2024)

Abstract

Objective Natural CD4+CD25+FoxP3+ Treg cells play a crucial role in maintaining immune homeostasis and controlling autoimmunity. In patients with juvenile idiopathic arthritis (JIA), inflammation occurs despite the increased total numbers of Treg cells in the synovial fluid (SF) compared to the peripheral blood (PB). This study was undertaken to investigate the phenotype of CD4+ T cells in PB and SF from JIA patients, the function of synovial Treg cells, and the sensitivity of PB and SF CD4+CD25- effector T cells to the immunoregulatory properties of Treg cells, and to study the suppression of cytokine secretion from SF effector T cells by Treg cells. Methods The phenotypes of effector T cells and Treg cells of PB and SF from JIA patients and healthy donors were determined by flow cytometry. The functionality of isolated Treg cells and effector T cells was quantified in 3H-thymidine proliferation assays. Cytokine levels were analyzed using Bio-Plex Pro assay. Results Compared to PB, SF showed significantly elevated numbers of activated and differentiated CD4+CD45RO+ T cells. Sensitivity of SF effector T cells to the suppressive effects of Treg cells from both PB and SF was impaired, correlating inversely with the expression of CD69 and HLA-DR. However, SF effector T cell cytokine secretion was partly suppressed by SF Treg cells. Conclusion Our findings indicate that regulation is impaired in the SF of patients with JIA, as shown by the resistance of effector T cells to immunoregulation by functional Treg cells. This resistance of the SF effector T cells might be due to their activated phenotype.

Original languageEnglish
Pages (from-to)3153-3162
Number of pages10
JournalArthritis and Rheumatism
Volume63
Issue number10
DOIs
StatePublished - Oct 2011
Externally publishedYes

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Haufe, S., Haug, M., Schepp, C., Kuemmerle-Deschner, J., Hansmann, S., Rieber, N., Tzaribachev, N., Hospach, T., Maier, J., Dannecker, G. E., & Holzer, U. (2011). Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells. Arthritis and Rheumatism, 63(10), 3153-3162. https://doi.org/10.1002/art.30503

Haufe, Susanne ; Haug, Markus ; Schepp, Carsten et al. / Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells. In: Arthritis and Rheumatism. 2011 ; Vol. 63, No. 10. pp. 3153-3162.

@article{612e29ec4d0b4d949252bd8a44c20deb,

title = "Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells",

abstract = "Objective Natural CD4+CD25+FoxP3+ Treg cells play a crucial role in maintaining immune homeostasis and controlling autoimmunity. In patients with juvenile idiopathic arthritis (JIA), inflammation occurs despite the increased total numbers of Treg cells in the synovial fluid (SF) compared to the peripheral blood (PB). This study was undertaken to investigate the phenotype of CD4+ T cells in PB and SF from JIA patients, the function of synovial Treg cells, and the sensitivity of PB and SF CD4+CD25- effector T cells to the immunoregulatory properties of Treg cells, and to study the suppression of cytokine secretion from SF effector T cells by Treg cells. Methods The phenotypes of effector T cells and Treg cells of PB and SF from JIA patients and healthy donors were determined by flow cytometry. The functionality of isolated Treg cells and effector T cells was quantified in 3H-thymidine proliferation assays. Cytokine levels were analyzed using Bio-Plex Pro assay. Results Compared to PB, SF showed significantly elevated numbers of activated and differentiated CD4+CD45RO+ T cells. Sensitivity of SF effector T cells to the suppressive effects of Treg cells from both PB and SF was impaired, correlating inversely with the expression of CD69 and HLA-DR. However, SF effector T cell cytokine secretion was partly suppressed by SF Treg cells. Conclusion Our findings indicate that regulation is impaired in the SF of patients with JIA, as shown by the resistance of effector T cells to immunoregulation by functional Treg cells. This resistance of the SF effector T cells might be due to their activated phenotype.",

author = "Susanne Haufe and Markus Haug and Carsten Schepp and Jasmin Kuemmerle-Deschner and Sandra Hansmann and Nikolaus Rieber and Nikolay Tzaribachev and Toni Hospach and Jan Maier and Dannecker, {Guenther E.} and Ursula Holzer",

year = "2011",

month = oct,

doi = "10.1002/art.30503",

language = "English",

volume = "63",

pages = "3153--3162",

journal = "Arthritis and Rheumatism",

issn = "0004-3591",

publisher = "John Wiley & Sons Inc.",

number = "10",

}

Haufe, S, Haug, M, Schepp, C, Kuemmerle-Deschner, J, Hansmann, S, Rieber, N, Tzaribachev, N, Hospach, T, Maier, J, Dannecker, GE & Holzer, U 2011, 'Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells', Arthritis and Rheumatism, vol. 63, no. 10, pp. 3153-3162. https://doi.org/10.1002/art.30503

Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells. / Haufe, Susanne; Haug, Markus; Schepp, Carsten et al.
In: Arthritis and Rheumatism, Vol. 63, No. 10, 10.2011, p. 3153-3162.

Research output: Contribution to journalArticlepeer-review

TY - JOUR

T1 - Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells

AU - Haufe, Susanne

AU - Haug, Markus

AU - Schepp, Carsten

AU - Kuemmerle-Deschner, Jasmin

AU - Hansmann, Sandra

AU - Rieber, Nikolaus

AU - Tzaribachev, Nikolay

AU - Hospach, Toni

AU - Maier, Jan

AU - Dannecker, Guenther E.

AU - Holzer, Ursula

PY - 2011/10

Y1 - 2011/10

N2 - Objective Natural CD4+CD25+FoxP3+ Treg cells play a crucial role in maintaining immune homeostasis and controlling autoimmunity. In patients with juvenile idiopathic arthritis (JIA), inflammation occurs despite the increased total numbers of Treg cells in the synovial fluid (SF) compared to the peripheral blood (PB). This study was undertaken to investigate the phenotype of CD4+ T cells in PB and SF from JIA patients, the function of synovial Treg cells, and the sensitivity of PB and SF CD4+CD25- effector T cells to the immunoregulatory properties of Treg cells, and to study the suppression of cytokine secretion from SF effector T cells by Treg cells. Methods The phenotypes of effector T cells and Treg cells of PB and SF from JIA patients and healthy donors were determined by flow cytometry. The functionality of isolated Treg cells and effector T cells was quantified in 3H-thymidine proliferation assays. Cytokine levels were analyzed using Bio-Plex Pro assay. Results Compared to PB, SF showed significantly elevated numbers of activated and differentiated CD4+CD45RO+ T cells. Sensitivity of SF effector T cells to the suppressive effects of Treg cells from both PB and SF was impaired, correlating inversely with the expression of CD69 and HLA-DR. However, SF effector T cell cytokine secretion was partly suppressed by SF Treg cells. Conclusion Our findings indicate that regulation is impaired in the SF of patients with JIA, as shown by the resistance of effector T cells to immunoregulation by functional Treg cells. This resistance of the SF effector T cells might be due to their activated phenotype.

AB - Objective Natural CD4+CD25+FoxP3+ Treg cells play a crucial role in maintaining immune homeostasis and controlling autoimmunity. In patients with juvenile idiopathic arthritis (JIA), inflammation occurs despite the increased total numbers of Treg cells in the synovial fluid (SF) compared to the peripheral blood (PB). This study was undertaken to investigate the phenotype of CD4+ T cells in PB and SF from JIA patients, the function of synovial Treg cells, and the sensitivity of PB and SF CD4+CD25- effector T cells to the immunoregulatory properties of Treg cells, and to study the suppression of cytokine secretion from SF effector T cells by Treg cells. Methods The phenotypes of effector T cells and Treg cells of PB and SF from JIA patients and healthy donors were determined by flow cytometry. The functionality of isolated Treg cells and effector T cells was quantified in 3H-thymidine proliferation assays. Cytokine levels were analyzed using Bio-Plex Pro assay. Results Compared to PB, SF showed significantly elevated numbers of activated and differentiated CD4+CD45RO+ T cells. Sensitivity of SF effector T cells to the suppressive effects of Treg cells from both PB and SF was impaired, correlating inversely with the expression of CD69 and HLA-DR. However, SF effector T cell cytokine secretion was partly suppressed by SF Treg cells. Conclusion Our findings indicate that regulation is impaired in the SF of patients with JIA, as shown by the resistance of effector T cells to immunoregulation by functional Treg cells. This resistance of the SF effector T cells might be due to their activated phenotype.

UR - http://www.scopus.com/inward/record.url?scp=80053493638&partnerID=8YFLogxK

U2 - 10.1002/art.30503

DO - 10.1002/art.30503

M3 - Article

C2 - 21702013

AN - SCOPUS:80053493638

SN - 0004-3591

VL - 63

SP - 3153

EP - 3162

JO - Arthritis and Rheumatism

JF - Arthritis and Rheumatism

IS - 10

ER -

Haufe S, Haug M, Schepp C, Kuemmerle-Deschner J, Hansmann S, Rieber N et al. Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells. Arthritis and Rheumatism. 2011 Oct;63(10):3153-3162. doi: 10.1002/art.30503

Impaired suppression of synovial fluid CD4+CD25- T cells from patients with juvenile idiopathic arthritis by CD4+CD25+ Treg cells (2024)

FAQs

Is juvenile idiopathic arthritis fatal? ›

Cumulative mortality in JIA was 0.6% (95% Cl 0.3-1.2) compared to 0.6% (95% Cl 0.4-1.0) in the controls; (hazard ratio 1.44, 95% Cl 0.70-2.95). Accidents were the most common (54%) cause of death in JIA, whereas suicide (39%) in the controls.

What is the disease SoJIA? ›

Systemic-onset juvenile idiopathic arthritis (SoJIA) is a systemic inflammatory disease which has up to now been classified as a category of juvenile idiopathic arthritis.

Is juvenile idiopathic arthritis a disability? ›

In short, juvenile arthritis can be considered a disability, but not every kid with JA is disabled.

What happens if juvenile idiopathic arthritis goes untreated? ›

If it is not treated, JIA can lead to: Permanent damage to joints. Interference with a child's bones and growth. Chronic (long-term) arthritis and disability (loss of function)

Is RA a serious autoimmune disease? ›

Rheumatoid arthritis is an autoimmune disease. Normally, your immune system helps protect your body from infection and disease. In rheumatoid arthritis, your immune system attacks healthy tissue in your joints. It can also cause medical problems with your heart, lungs, nerves, eyes and skin.

Is juvenile idiopathic arthritis a rare disease? ›

Juvenile idiopathic arthritis (JIA) is the most common type of arthritis in kids and teens. About 10% to 20% of children with JIA have a rare and serious subtype called systemic juvenile idiopathic arthritis (SJIA).

Can you be cured of RA? ›

Although there's no cure for rheumatoid arthritis, early treatment and support (including medicine, lifestyle changes, supportive treatments and surgery) can reduce the risk of joint damage and limit the impact of the condition. Your treatment will usually involve care from your GP and several different specialists.

Can you live a normal life with JIA? ›

With treatment, 50 to 70 percent of children with JIA go into remission. If caught and treated early, most children live normal, active lives.

Does JIA get worse over time? ›

Nearly half of all children with JIA recover fully. Others may have symptoms for years. Some will have rashes and fever. Others may have arthritis that gets worse.

What triggers juvenile idiopathic arthritis? ›

While the exact causes of JIA are unknown, it begins when the immune system becomes overactive and creates inflammation. With treatment, most children achieve periods of wellness (remission), and sometimes the disease goes away permanently with no further need for medications.

Can you outgrow juvenile idiopathic arthritis? ›

Many children with pauciarticular disease outgrow arthritis by adulthood, although eye problems can continue and joint symptoms may recur in some people. About 30% of all children with JRA have polyarticular disease, in which five or more joints are affected.

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