New regulatory CD19+CD25+ B-cell subset in clinically isolated syndrome and multiple sclerosis relapse. Changes after glucocorticoids

Andrés, Clara de; Tejera-Alhambra, Marta; Alonso, Bárbara; Valor, Lara; Teijeiro, Roseta; Ramos-Medina, Rocío; Mateos, Dolores; Faure, Florence; Sánchez-Ramón, Silvia

doi:10.1016/j.jneuroim.2014.02.003

Cited by 48 publications

(33 citation statements)

References 44 publications

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“…The authors assumed that the observed high proportion of circulating CD19+CD25hig FoxP3high Bregs in MS patients during relapse was a compensatory peripheral response to the inflammatory circumstances of disease activity. The involvement of Bregs highly expressing FoxP3both in PB and CSF of MS patients is relevant to understanding the pathogenesis of MS and to the follow-up of diseases activity following immunosuppressive therapies [65]. Two less-studied Breg cell subsets (CD19+FoxP3+ and CD19+TGF-β+) were recently assessed in patients suffering from RA aiming to see if this was in association with disease activity and or the incidence of interstitial lung disease (ILD).…”

Section: Foxp3 Expression In Macrophagesmentioning

confidence: 99%

FoxP3 Expression in Macrophages, Cancer, and B Cells—Is It Real?

Vadasz

Toubi

2016

Clinic Rev Allerg Immunol

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During the last decade, B regulatory cells are appreciated to have a central role in preventing autoimmunity and maintaining self-tolerance. They are characterized by expressing different phenotypic markers and the production of either IL-10 or TGF-β or both. The recent recognition of Fas ligand expressing B regulatory cells as "killer" cells established their role in maintaining viral persistence by preventing effective antiviral immune responses. The forkhead lineage-transcription factor (FoxP3) was considered for many years to be a highly specific intracellular regulatory marker of CD4+CD25+ T regulatory cells. The possibility of FoxP3 being expressed in B regulatory cells was suggested in many studies. Though controversial, FoxP3 expression was also reported in macrophages and cancer cells. Aiming to avoid artifact staining, many researchers required the usage of FoxP3 messenger RNA (mRNA) and PCR in order to prove a true expression of FoxP3 in these different cells. In addition, most studies' report on that FoxP3 expression in all abovementioned cells is related to their status of activation since naïve (non-activated cells) were found poorly FoxP3 expressing. In this review, we present the existing data on FoxP3 expression in non-T-regulatory cells, but we suggest that further studies are needed to better establish this concept.

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Section: Foxp3 Expression In Macrophagesmentioning

confidence: 99%

FoxP3 Expression in Macrophages, Cancer, and B Cells—Is It Real?

Vadasz

Toubi

2016

Clinic Rev Allerg Immunol

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“…15 Variously described as CD19 C CD38 high CD24 high or CD19 C CD25 high B cells, Breg in humans regulate functions of Th1 helper cells by producing immunosuppressive IL-10 or degranulation of perforin/granzyme molecules, respectively. 16,17 The antibody-independent regulation of T-cell functions by B cells is of great interest, largely because of the potential involvement of Breg in inflammation, autoimmune diseases and cancer. 18,19 Functional impairments of CD19 C CD38 high CD24 high Breg in systemic lupus erythematosus (SLE) patients 17 and an increased frequency of CD19 C CD25 high Breg during clinical manifestations of multiple sclerosis 16 illustrate their role in autoimmune diseases.…”

Section: Introductionmentioning

confidence: 99%

Phenotypic and functional characteristics of CD39^highhuman regulatory B cells (Breg)

et al. 2016

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CD39 and CD73 are key enzymes in the adenosine (ADO) pathway. ADO modulates pathophysiological responses of immune cells, including B cells. It has recently emerged that a subpopulation of ADOproducing CD39 C CD73 C B cells has regulatory properties. Here, we define the CD39 high subset of these cells as the major contributor to the regulatory network operated by human B lymphocytes. Peripheral blood B cells were sorted into CD39 neg , CD39 inter and CD39 high subsets. The phenotype, proliferation and IL-10 secretion by these B cells were studied by flow cytometry. 5 0 -AMP and ADO levels were measured by mass spectrometry. Agonists or antagonists of A 1 R, A 2A R and A 3 R were used to study ADO-

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“…In humans, B reg cells have been phenotyped using CD24, IL-10, and Fox-P3 markers (35) (6, 34). As we were not able to identify reliable antibody clones that recognized CD24 in macaques we identified B reg cells as CD19 + CD25 high as previously described (5, 6).…”

Section: Resultsmentioning

confidence: 99%

“…They can act as antigen presenting cells and also as effector cells, producing antibodies, cytokines, adhesion molecules and chemokines (2–4). They have been reported to exert immune suppressive effects (5, 6) and to regulate T cell immunity in chronic hepatitis B infection and to impair CTL activity during HIV infection (7, 8). Both HIV and SIV infections lead to severe B-cell dysregulation and dysfunction in their respective hosts (9, 10).…”

Section: Introductionmentioning

confidence: 99%

B Cell Responses Associated with Vaccine-Induced Delayed SIVmac251 Acquisition in Female Rhesus Macaques

Mohanram

Demberg

Musich

et al. 2016

The Journal of Immunology

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An established sex bias in HIV pathogenesis is linked to immune responses. Recently we reported a vaccine-induced sex bias: vaccinated female but not male rhesus macaques exhibited delayed SIV acquisition. This outcome was correlated with SIV Env-specific rectal IgA, rectal memory B cells, and total rectal plasma cells (PC). To uncover additional contributing factors, using samples from the same study we investigated memory B cell population dynamics in blood, bone marrow (BM) and rectal tissue during immunization and post-challenge; IgG subtypes and antibody avidity; and Breg cell frequency and function. Few sex differences were seen in Env-specific memory B cell, plasmablast or PC frequencies in the three compartments. Males had higher IgG antibody titers and avidity indices than females. However, females had elevated levels of Env-specific IgG1, IgG2, and IgG3 antibodies compared to males. gp140-specific IgG3 antibodies of females but not males were correlated with ADCC activity against gp120 targets (p = 0.026) and with antibody-dependent phagocytic activity (p = 0.010). IgG3 antibody of females but not males also correlated with decreased peak viremia (p = 0.028). Peripheral blood CD19+CD25+ Breg cells suppressed T cell proliferation compared to CD19+CD25− cells (p=0.031), and exhibited increased IL-10 mRNA expression (p=0.031). Male macaques post-vaccination (p=0.018) and post-infection (p=0.0048) exhibited higher Breg frequencies than females. Moreover, male Breg frequencies correlated with peak viremia (p=0.0071). Our data suggest that vaccinated females developed better antibody quality, contributing to better functionality. The elevated Breg frequencies in males may have facilitated SIV acquisition.

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New regulatory CD19+CD25+ B-cell subset in clinically isolated syndrome and multiple sclerosis relapse. Changes after glucocorticoids

Cited by 48 publications

References 44 publications

FoxP3 Expression in Macrophages, Cancer, and B Cells—Is It Real?

FoxP3 Expression in Macrophages, Cancer, and B Cells—Is It Real?

Phenotypic and functional characteristics of CD39^highhuman regulatory B cells (Breg)

B Cell Responses Associated with Vaccine-Induced Delayed SIVmac251 Acquisition in Female Rhesus Macaques

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New regulatory CD19+CD25+ B-cell subset in clinically isolated syndrome and multiple sclerosis relapse. Changes after glucocorticoids

Cited by 48 publications

References 44 publications

FoxP3 Expression in Macrophages, Cancer, and B Cells—Is It Real?

FoxP3 Expression in Macrophages, Cancer, and B Cells—Is It Real?

Phenotypic and functional characteristics of CD39highhuman regulatory B cells (Breg)

B Cell Responses Associated with Vaccine-Induced Delayed SIVmac251 Acquisition in Female Rhesus Macaques

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Phenotypic and functional characteristics of CD39^highhuman regulatory B cells (Breg)