Tolerogenic property of B-1b cells in a model of allergic reaction

Lorenzo, Beatriz Helena Pizarro De; Brito, Rosineide Santana de; Godoy, Luiz C.; Lopes, José Daniel; Mariano, Mário

doi:10.1016/j.imlet.2007.09.013

Cited by 28 publications

(28 citation statements)

References 33 publications

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“…mice. However, MyD88 signaling is not only involved in the TLR9-dependent development of anti-nucleosome IgG2c and IgG2b autoantibodies but also in cell maturation via other TLRs (e.g., TLR7) (7-12, 14, 15, 17, 40, 41 analyzed by CD5 expression at day 7. that B-1b cells have a tolerogenic function, but underlying mechanisms have been unknown (44,45 Taken together, our data suggest that the tolerogenic function of MyD88-dependent TLR9 signaling is mediated by the production of self-reactive serum IgM Abs by peritoneal B-1b cells, which protects from uncontrolled accumulation of Th17 cells and severe autoimmunity. These findings provide new insight in the tolerogenic function of TLR9, B-1b cells, and self-reactive IgM to control autoimmunity and have implications for the development of TLR ligand-dependent therapies and B cell depletion protocols as a treatment for autoimmunity.…”

Section: Monoclonal Self-reactive Igm Abs Reduce Th17 Cell Accumulatimentioning

confidence: 75%

TLR9 in Peritoneal B-1b Cells Is Essential for Production of Protective Self-Reactive IgM To Control Th17 Cells and Severe Autoimmunity

Stoehr

Schoen

Mertes

et al. 2011

The Journal of Immunology

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The role of TLR9 in the development of the autoimmune disease systemic lupus erythematosus is controversial. In different mouse models of the disease, loss of TLR9 abolishes the generation of anti-nucleosome IgG autoantibodies but at the same time exacerbates lupus disease. However, the TLR9-dependent tolerance mechanism is unknown. In this study, we show that loss of TLR9 is associated with low peritoneal B-1b cell numbers and low levels of protective self-reactive IgM serum autoantibodies in lupus-prone FcγRIIB-deficient mice leading to the uncontrolled accumulation of proinflammatory CD4+ cells and exacerbated autoimmunity. TLR7 signaling was not able to compensate for the loss of TLR9 signaling in peritoneal B-1b cells to induce IgM Abs. Transfer of TLR9-expressing peritoneal B-1b cells from FcγRIIB-deficient mice or of recombinant monoclonal self-reactive IgM Abs was sufficient to reduce the frequency of proinflammatory Th17 cells and lupus disease in FcγRIIB/TLR9 double-deficient mice. Taken together, these data provide evidence for a TLR9-dependent tolerance mechanism of peritoneal B-1b cells generating protective self-reactive IgM in lupus-prone mice to control Th17 cell development and severe autoimmunity.

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Section: Monoclonal Self-reactive Igm Abs Reduce Th17 Cell Accumulatimentioning

confidence: 75%

TLR9 in Peritoneal B-1b Cells Is Essential for Production of Protective Self-Reactive IgM To Control Th17 Cells and Severe Autoimmunity

Stoehr

Schoen

Mertes

et al. 2011

The Journal of Immunology

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“…well established. It has also been demonstrated that these cells facilitate parasite infectivity 26) , promote tumor growth 19,20) , have tolerogenic properties 18) , are radiosensitive 13) , migrate from the peritoneal cavity to distant inflammatory lesions and differentiate into a mononuclear phagocyte 14,16) . Nevertheless, there are no reports in the literature considering the possible existence of B-1 cells in the peritoneal and pleural cavities of rabbits.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, having been completely destroyed by ionizing radiation, the cells repopulated the peritoneal cavity in 45 days in mice 13,14) . Further, B-1 cells participate in the genesis of inflammatory giant cells 17) , are endowed with tolerogenic properties 18) and facilitate the growth and metastatic potential of experimental melanoma 19,20) . e Brito et al 13) demonstrated that, in this particular model of SLE (NZB/NZW) F1 mice, irradiation significantly halted the development of SLE, even though B-1 cells seemed not to be affected by radiation in (NZB/NZW) F1 mice.…”

Section: Introductionmentioning

confidence: 99%

Resident Peritoneal Inflammatory Cells are Pivotal in the Development of Experimental Atherosclerosis

Relvas

Izar

Segreto

et al. 2010

JAT

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Aim: Based on evidence that ionizing radiation can ameliorate chronic and autoimmune diseases in patients and experimental animals, we investigated the effects of radiation on the induction and development of experimental atherogenesis. Methods: Male New Zealand rabbits were divided into 5 groups and given an atherogenic diet for 90 days. Peritoneal and thoracic areas (9 Gy) were irradiated on the 1st and 45th days for groups 1 and 2, the 45th day for groups 3 and 4, and not at all for group 5. Prior to irradiation, the peritoneal cavity of animals from groups 1 and 3 was washed with buffered saline. Cells collected by peritoneal washing were reinfused into the peritoneal cavity of the same animal after irradiation. Animals from groups 2 and 4 were intraperitoneally injected with saline as a control. Results: Despite similar lipid profiles among the experimental groups, the percentage of aortas covered by plaques was remarkably reduced (p 0.001) among animals submitted to irradiation (groups 2 and 4). These differences were completely abolished in irradiated animals reconstituted with their own peritoneal cells.

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“…This population of cells is found mainly in the peritoneal and pleural cavities in mice, and they are rarely found in the spleen and are not detected in lymph nodes. They are typically IgM 3,4 It is known that B-1 cells are able to migrate from the peritoneal cavity to non-specific inflammatory sites in mice; 5,6 in addition, these cells differentiate into phagocyte-like cells in vitro. These phagocyte-like cells are capable of ingesting mannose-coated particles, 6 and they are also able to phagocytose and kill bacteria in culture.…”

Section: Introductionmentioning

confidence: 99%

In Vitro and In Vivo Phagocytic Ability of Mouse B-1 Cells

Brito

Cortez

Machado-Santelli

et al. 2010

Immunol Immunogenet Insights

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B-1 cells are a peculiar subpopulation of B cells found in the peritoneal and pleural cavities in mice. These cells are typically IgM + and CD11b +. B-1 cells are able to migrate from the peritoneal cavity to non-specific inflammatory sites in mice. In addition, they can differentiate into mononuclear phagocyte-like cells in vitro; however, it is still unknown whether B-1 cells are capable of performing phagocytosis in vivo. Here we further characterized B-1 cells as phagocytes in vitro, and we investigated their ability to phagocytose apoptotic cells and bacteria in vivo. Our results demonstrate that B-1 phagocytes are able to uptake apoptotic thymocytes and Escherichia coli bacteria, both in vitro and in vivo. These findings indicate that along with macrophages, B-1 phagocytic cells might play a role in fundamental processes such as tissue remodeling, resolution of inflammation and pathogen clearance.

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Tolerogenic property of B-1b cells in a model of allergic reaction

Cited by 28 publications

References 33 publications

TLR9 in Peritoneal B-1b Cells Is Essential for Production of Protective Self-Reactive IgM To Control Th17 Cells and Severe Autoimmunity

TLR9 in Peritoneal B-1b Cells Is Essential for Production of Protective Self-Reactive IgM To Control Th17 Cells and Severe Autoimmunity

Resident Peritoneal Inflammatory Cells are Pivotal in the Development of Experimental Atherosclerosis

In Vitro and In Vivo Phagocytic Ability of Mouse B-1 Cells

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