Human T cells induce their own regulation through activation of B cells

Lemoine, Sébastien; Morva, Ahsen; Youinou, Pierre; Jamin, Christophe

doi:10.1016/j.jaut.2011.01.005

Cited by 136 publications

(128 citation statements)

References 43 publications

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“…24 Although we detected a significant concentration of Bregs in the CD27 1 B-cell compartment, we could not replicate the findings of specific enrichment either in the transitional or in the CD5 1 B-cell compartment as previously described. 55,56 Several factors may explain these discrepancies. First, our study was focused on cGVHD patients and included a higher number of patients: 47 patients vs 11 in the study by Khoder et al Second, the stimulations used to study B-cell IL-10 production were different.…”

mentioning

confidence: 99%

CD24hiCD27+ and plasmablast-like regulatory B cells in human chronic graft-versus-host disease

Masson

Bouaziz

Buanec

et al. 2015

Blood

146

119

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Key Points• Chronic graft-versus-host disease is associated with a global Breg defect.• This defect is particularly accentuated in the CD24 hi CD27 1 Breg compartment.Interleukin 10 (IL-10)-producing B cells (regulatory B cells [Bregs]) regulate autoimmunity in mice and humans, and a regulatory role of IL-10-producing plasma cells has been described in mice. Dysfunction of B cells that maintain homeostasis may play a role in the pathogenesis of chronic graft-versus-host disease (cGVHD) after allogeneic stem cell transplantation. Here, we found a relation between decreased Breg frequencies and cGVHD severity. An impaired ability of B cells to produce IL-10, possibly linked to poor signal transducer and activator of transcription 3 and extracellular signal-regulated kinase phosphorylation, was found in patients with active cGVHD. IL-10 production was not confined to a single B-cell subset, but enriched in both the CD24 hi CD27 1 and CD27 hi CD38 hi plasmablast B-cell compartments. In vitro plasmablast differentiation increased the frequency of IL-10-producing B cells. We confirmed that allogeneic transplant recipients had an impaired reconstitution of the memory B-cell pool. cGVHD patients had less CD24 hi CD27 1 B cells and IL-10-producing CD24 hi CD27 1 B cells. Patients with cGVHD had increased plasmablast frequencies but decreased IL-10-producing plasmablasts. These results suggest a role of CD24 hi CD27 1 B-cell and plasmablast-derived IL-10 in the regulation of human cGVHD. (Blood. 2015;125(11):1830-1839 IntroductionChronic graft-versus-host disease (cGVHD) is the leading cause of morbi-mortality after allogeneic hematopoietic stem cell transplantation (AHSCT). 1 GVHD prevention by means of adoptive transfer of regulatory T cells (Tregs) 2,3 and cGVHD treatment by in vivo induction of Tregs by low-dose interleukin 2 (IL-2) 4,5 may be effective. The exact role of IL-10-producing regulatory B cells (Bregs) in cGVHD is yet to be understood. Bregs have been shown to downmodulate adaptive 6 or innate immune responses 7 in mice and humans. In cGVHD, B cells are essentially recognized as positive regulators of inflammation. 1,8,9 Increased B-cell receptor responsiveness was found in cGVHD patients. 10 B-cell homeostatic defects were described in cGVHD, including elevated B-cell activating factor of the tumor necrosis factor (TNF) family (BAFF)/B-cell ratios, 11-15 expansion of CD21 lo B cells, 16 reduced CD5 1 B1-like cell numbers, 17 decreased CD27 1 memory B cells, and hypogammaglobulinemia. 18 BAFF concentrations correlated with increased circulating pre-germinal center (GC) B-cell and post-GC plasmablast cell counts in patients with cGVHD. 11 B-cell depletion with rituximab prevented cGVHD in humans. 19 Patients with cGVHD frequently have circulating antibodies reactive to recipient cells. 1,9,20 Besides their functions in antibody secretion, cytokine and chemokine production, and antigen presentation, B cells exhibit regulatory properties in several human autoimmune diseases including systemic lupus erythemat...

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mentioning

confidence: 99%

CD24hiCD27+ and plasmablast-like regulatory B cells in human chronic graft-versus-host disease

Masson

Bouaziz

Buanec

et al. 2015

Blood

146

119

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“…effector T cells, including cytokines such as TGF-b and IL-10 [33]. Bregs are also capable of directly inducing anergy of Th1 cells, CD8, and CD4 T cells [34] or indirectly by converting Tregs [19,22]. Some studies indicated that the Tregs immunosuppressive role in tumors is mediated by Bregs [35].…”

Section: Discussionmentioning

confidence: 99%

“…CD25 ? T cells [18,19]. Further evidences suggested that these Bregs play an essential role in pathogenesis of autoimmune diseases [16].…”

Section: Introductionmentioning

confidence: 99%

The correlation of CD19 + CD24 + CD38 + B cells and other clinicopathological variables with the proportion of circulating Tregs in breast cancer patients

et al. 2017

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“…Kod pojedinih modela, kao što su artritis i hronični kolitis, deplecija B limfocita je pogoršala kliničku sliku bolesti, što je ukazalo na njihovu regulatornu ulogu. 2 Kod nekih modela je deplecija B limfocita u različitim fazama razvoja bolesti imala suprotne efekte na razvoj kliničke slike bolesti. Ubedljive dokaze o ulozi B limfocita u T zavisnom imunskom odgovoru su pružile studije privremene deplecije, u kojima je razdvojena uloga B limfocita u fazi inicijacije i razvoja, i fazi efektorske funkcije imunskog odgovora.…”

Section: Uvodunclassified

Role of B cells in the development of multiple sclerosis and experimental autoimmune encephalomyelitis

Jovičić¹,

Jeftic²,

Jovicic³

2013

PONS

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Human T cells induce their own regulation through activation of B cells

Cited by 136 publications

References 43 publications

CD24hiCD27+ and plasmablast-like regulatory B cells in human chronic graft-versus-host disease

CD24hiCD27+ and plasmablast-like regulatory B cells in human chronic graft-versus-host disease

The correlation of CD19 + CD24 + CD38 + B cells and other clinicopathological variables with the proportion of circulating Tregs in breast cancer patients

Role of B cells in the development of multiple sclerosis and experimental autoimmune encephalomyelitis

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