Regulatory B cells prevent and reverse allergic airway inflammation via FoxP3-positive T regulatory cells in a murine model

Amu, Sylvie; Saunders, Sean P.; Kronenberg, Mitchell; Mangan, Niamh E.; Atzberger, Ann; Fallon, Padraic G.

doi:10.1016/j.jaci.2010.01.018

Cited by 325 publications

(342 citation statements)

References 76 publications

(6 reference statements)

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“…Fluorescent mAbs to mouse leukocyte surface molecules used in flow cytometric analysis, B220 (RA3-6B2), CD21/35 (4E3), CD23 (B3B4), CD5 (53-7.3), CD1d (1B1), IgM (eB121-15F9), IgD (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26), CD3 (145-2C11), CD4 (L3T4), CD8 (53-6.7), CD49b (DX5), CD19 (1D3), and Treg-cell staining kit were purchased from eBioscience (CA, USA). PE-conjugated anti-mouse IL-10 mAb (JES5-16E3) was obtained from BD Biosciences.…”

Section: Flow Cytometrymentioning

confidence: 99%

Role of IL‐10‐producing regulatory B cells in control of cerebral malaria in Plasmodium berghei infected mice

Liu

Chen

et al. 2013

Eur J Immunol

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IntroductionMalaria caused by infection with protozoan parasites of Plasmodium spp. is one of the most serious infectious diseases of humans and causes about one million deaths annually. Plasmodium infection may induce multiple disease syndromes including severe anemia, metabolic acidosis, and neurological dysfunction, e.g. cerebral malaria (CM) [1]. Sequestration of the Correspondence: Dr. Zhong Su e-mail: su_zhong@gibh.ac.cn parasitized red blood cells (pRBCs) in brain microvessels is a characteristic histopathology feature observed in human and murine CM and is believed to be the primary cause of the neurological syndrome [2,3]. Evidence from more recent studies supports the notion that CM is an immune-driven pathology. The proinflammatory cytokines and mediators produced in the "cytokine storm" during malaria induce activation and recruitment of cytotoxic CD8 + cells in brain blood vessels and upregulate the expression of adhesion receptors by brain endothelial cells, leading to leukocyte accumulation and capillary obstruction, cerebral hemorrhage, and hypoxia in brain tissues [1,[4][5][6]. Therefore, the immune regulatory cells and cytokines may be critical in counteracting the inflammatory response and prevention of malaria-associated www.eji-journal.eu 2908 Yunfeng Liu et al. Eur. J. Immunol. 2013. 43: 2907-2918 neuropathology. The levels of anti-inflammatory cytokines such as IL-10 and TGF-β have been shown to be inversely associated with the occurrence of CM in murine malaria [7,8]. However, no consensus has been reached concerning the role of regulatory T (Treg) cells in regulation of CM pathogenesis [9][10][11].B cells have been traditionally considered antibody-producing cell and APC. Many studies in recent years showed the existence of a subset of B cells that exhibit the immune regulatory functions (reviewed in [12]). An early study by Fillatreau et al.[13] reported a subset of B cells that produce IL-10 and inhibit the immune pathology in murine EAE. Further studies revealed that these regulatory B (Breg) cells play important roles in control of immunopathology in autoimmune diseases [14], cancer [15], and organ transplantation [16]. Breg cells have also been shown to modulate immune responses and immunopathology in infectious diseases. Protective immunities against Salmonella typhimurium and Brucella abortus infections were inhibited by transfer of Breg cells in mouse models [17,18]. Transfer of CD1d + CD5 hi Breg cells rendered the BALB/c mice more susceptible to Leishmania major infection [19]. Adoptive transfer of IL-10-producing B cells isolated from helminth-infected mice inhibited the allergic responses and autoimmune inflammation in recipient mice [20]. Thus, Breg cells are an important component of immunoregulatory system and plays critical roles in immune homeostasis.The immunomodulatory roles of Breg cells have been studied in autoimmune and infectious disease settings, but little is known of its role in regulation of immune response and immunopathology of malaria. In this study, we i...

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Section: Flow Cytometrymentioning

confidence: 99%

Role of IL‐10‐producing regulatory B cells in control of cerebral malaria in Plasmodium berghei infected mice

Liu

Chen

et al. 2013

Eur J Immunol

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“…pDCs can drive CD4 + T cells to become CD4 + CD25 + Foxp3 + cells, which are identified as Tregs (20,21). The role of Tregs in a tumor microenvironment can be translated into anergy and immunosuppression, favoring the immune escape of tumor cells with the concomitant increase of tumor burden (14,22).…”

Section: Low-dose Lps Facilitates An Immunosuppressive Environment Inmentioning

confidence: 99%

Plasmacytoid Dendritic Cells Play a Key Role in Tumor Progression in Lipopolysaccharide-Stimulated Lung Tumor–Bearing Mice

Rega

Terlizzi

Luciano

et al. 2013

The Journal of Immunology

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The antitumor activity of LPS was first described by Dr. William Coley. However, its role in lung cancer remains unclear. The aim of our study was to elucidate the dose-dependent effects of LPS (0.1–10 μg/mouse) in a mouse model of B16-F10–induced metastatic lung cancer. Lung tumor growth increased at 3 and 7 d after the administration of low-dose LPS (0.1 μg/mouse) compared with control mice. This was associated with an influx of plasmacytoid dendritic cells (pDCs), regulatory T cells, myeloid-derived suppressor cells, and CD8+ regulatory T cells. In contrast, high-dose LPS (10 μg/mouse) reduced lung tumor burden and was associated with a greater influx of pDCs, as well as a stronger Th1 and Th17 polarization. Depletion of pDCs during low-dose LPS administration resulted in a decreased lung tumor burden. Depletion of pDCs during high-dose LPS treatment resulted in an increased tumor burden. The dichotomy in LPS effects was due to the phenotype of pDCs, which were immunosuppressive after the low-dose LPS, and Th1- and T cytotoxic–polarizing cells after the high-dose LPS. Adoptive transfer of T cells into nude mice demonstrated that CD8+ T cells were responsible for pDC recruitment following low-dose LPS administration, whereas CD4+ T cells were required for pDC influx after the high-dose LPS. In conclusion, our data suggest differential effects of low-dose versus high-dose LPS on pDC phenotype and tumor progression or regression in the lungs of mice.

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“…In the past few years, several in vitro coculture experiments have shown that B cells have the ability to induce the generation of Treg cells and expand Foxp3 1 CD4 1 T cells in the absence of exogenous cytokines. [8][9][10] Antigen-loaded B cells isolated from Peyer's patches have also been shown to have the potential to induce suppressive Treg cells. 11 In the above-mentioned studies, purified splenic CD19 1 or B220 1 B-2 cells were investigated.…”

Section: Introductionmentioning

confidence: 99%

A B-1a cell subset induces Foxp3− T cells with regulatory activity through an IL-10-independent pathway

Hsu

Chu

et al. 2014

Cell Mol Immunol

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Regulatory B cells prevent and reverse allergic airway inflammation via FoxP3-positive T regulatory cells in a murine model

Cited by 325 publications

References 76 publications

Role of IL‐10‐producing regulatory B cells in control of cerebral malaria in Plasmodium berghei infected mice

Role of IL‐10‐producing regulatory B cells in control of cerebral malaria in Plasmodium berghei infected mice

Plasmacytoid Dendritic Cells Play a Key Role in Tumor Progression in Lipopolysaccharide-Stimulated Lung Tumor–Bearing Mice

A B-1a cell subset induces Foxp3− T cells with regulatory activity through an IL-10-independent pathway

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