Decreased Circulating CD28-negative T Cells in Patients with Rheumatoid Arthritis Treated with Abatacept Are Correlated with Clinical Response

Scarsi, Mirko; Ziglioli, Tamara; Airò, Paolo

doi:10.3899/jrheum.091176

Cited by 57 publications

(42 citation statements)

References 31 publications

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“…Scarsi et al have shown changes in populations of CD28-expressing CD8 T cells in abatacept-treated rheumatoid arthritis (16) and that the baseline number of circulating CD28-negative T cells predicts remission (17). These and our findings may be related, but CD28 was not incorporated into our current panel, and future studies will be needed to examine whether these observations align.…”

Section: Discussionmentioning

confidence: 99%

Reduction in CD4 Central Memory T-Cell Subset in Costimulation Modulator Abatacept-Treated Patients With Recent-Onset Type 1 Diabetes Is Associated With Slower C-Peptide Decline

Orban

Beam

et al. 2014

Diabetes

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We previously reported that continuous 24-month costimulation blockade by abatacept significantly slows the decline of β-cell function after diagnosis of type 1 diabetes. In a mechanistic extension of that study, we evaluated peripheral blood immune cell subsets (CD4, CD8-naive, memory and activated subsets, myeloid and plasmacytoid dendritic cells, monocytes, B lymphocytes, CD4+CD25high regulatory T cells, and invariant NK T cells) by flow cytometry at baseline and 3, 6, 12, 24, and 30 months after treatment initiation to discover biomarkers of therapeutic effect. Using multivariable analysis and lagging of longitudinally measured variables, we made the novel observation in the placebo group that an increase in central memory (CM) CD4 T cells (CD4+CD45R0+CD62L+) during a preceding visit was significantly associated with C-peptide decline at the subsequent visit. These changes were significantly affected by abatacept treatment, which drove the peripheral contraction of CM CD4 T cells and the expansion of naive (CD45R0−CD62L+) CD4 T cells in association with a significantly slower rate of C-peptide decline. The findings show that the quantification of CM CD4 T cells can provide a surrogate immune marker for C-peptide decline after the diagnosis of type 1 diabetes and that costimulation blockade may exert its beneficial therapeutic effect via modulation of this subset.

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Section: Discussionmentioning

confidence: 99%

Reduction in CD4 Central Memory T-Cell Subset in Costimulation Modulator Abatacept-Treated Patients With Recent-Onset Type 1 Diabetes Is Associated With Slower C-Peptide Decline

Orban

Beam

et al. 2014

Diabetes

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show abstract

“…However, Scarsi et al observed that the effect of anti-TNF-a treatment positively correlated with the clinical response [69]. The same group also showed that the baseline numbers of CD4 + CD28 -T cells in the blood of RA patients can predict the response to TNF-a inhibition [70].…”

Section: Viral Infectionsmentioning

confidence: 96%

Pathogenic features of CD4+CD28– T cells in immune disorders

Broux¹,

Marković-Pleše²,

Stinissen³

et al. 2012

Trends in Molecular Medicine

106

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“…Others demonstrated reduction of CD8+CD28- and late-stage CD8 effector memory, but not CD4+CD28- T-cells after 48 weeks of abatacept treatment. The decreases of CD28- cells among both CD4+ and CD8+ T lymphocyte populations after abatacept therapy were correlated with the clinical response as measured by DAS28/CRP [213]. Interestingly, the absolute numbers of CD28- T-cells (before treatment) were found to predict the response to abatacept [214].…”

Section: Effects Of Ra Treatment On the Aged Profile In Ramentioning

confidence: 99%

Rheumatoid Arthritis, Immunosenescence and the Hallmarks of Aging

Chalan¹,

Berg²,

Kroesen

et al. 2015

CAS

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Age is the most important risk factor for the development of infectious diseases, cancer and chronic inflammatory diseases including rheumatoid arthritis (RA). The very act of living causes damage to cells. A network of molecular, cellular and physiological maintenance and repair systems creates a buffering capacity against these damages. Aging leads to progressive shrinkage of the buffering capacity and increases vulnerability. In order to better understand the complex mammalian aging processes, nine hallmarks of aging and their interrelatedness were recently put forward.RA is a chronic autoimmune disease affecting the joints. Although RA may develop at a young age, the incidence of RA increases with age. It has been suggested that RA may develop as a consequence of premature aging (immunosenescence) of the immune system. Alternatively, premature aging may be the consequence of the inflammatory state in RA. In an effort to answer this chicken and egg conundrum, we here outline and discuss the nine hallmarks of aging, their contribution to the pre-aged phenotype and the effects of treatment on the reversibility of immunosenescence in RA.

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Decreased Circulating CD28-negative T Cells in Patients with Rheumatoid Arthritis Treated with Abatacept Are Correlated with Clinical Response

Abstract: After therapy with abatacept, circulating CD28- T cells and other effector populations decrease in patients with RA. This decrease is correlated with clinical response.

Cited by 57 publications

References 31 publications

Reduction in CD4 Central Memory T-Cell Subset in Costimulation Modulator Abatacept-Treated Patients With Recent-Onset Type 1 Diabetes Is Associated With Slower C-Peptide Decline

Reduction in CD4 Central Memory T-Cell Subset in Costimulation Modulator Abatacept-Treated Patients With Recent-Onset Type 1 Diabetes Is Associated With Slower C-Peptide Decline

Pathogenic features of CD4+CD28– T cells in immune disorders

Rheumatoid Arthritis, Immunosenescence and the Hallmarks of Aging

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