Induction of IL-10-Producing CD1dhighCD5+ Regulatory B Cells following Babesia microti-Infection

Jeong, Young-Il; Hong, Sung-Hee; Cho, Shin‐Hyeong; Lee, Won-Ja; Lee, Sang-Eun

doi:10.1371/journal.pone.0046553

Cited by 57 publications

(47 citation statements)

References 22 publications

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“…Instead intra-erythrocyte parasite death was associated with elevated levels of the anti-inflammatory cytokines IL-10, and G-CSF. Other studies of B. microti infection, like the current study, noted serum IL-10 production but also reported modest elevation of serum pro-inflammatory cytokines including IFN-γ (33, 34), which we did not observe. IL-12p40 was also elevated; this cytokine can form homodimers that may play an antagonistic role in the development of IL-12p70 responses, though this remains unclear.…”

Section: Discussioncontrasting

confidence: 73%

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Skariah

Arnaboldi

Dattwyler

et al. 2017

The Journal of Immunology

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Babesiosis is a tick-borne zoonosis caused by protozoans of the genus Babesia; apicomplexan parasites that replicate within erythrocytes. However, unlike related Plasmodium species, the pathogenesis of Babesia infection remains poorly understood. The primary etiological agent of babesiosis in the US is B. microti. In healthy individuals, tick transmitted infection with Babesia causes no specific clinical manifestations, with many having no symptoms at all. However, even in asymptomatic people, a Babesia carriage state can be established that can last up to a year or more. Current blood bank screening methods do not identify infected donors, and Babesia parasites survive blood banking procedures and storage. Thus, Babesia can also be transmitted by infected blood, and is currently the number one cause of reportable transfusion transmitted infection in the US. Despite a significant impact on human health, B. microti remains understudied. Here, we evaluated the course of Babesia infection in three different strains of mice, C57BL/6J, BALB/cJ and C3H-HeJ, and examined the contribution of multiple immune parameters including: toll-like receptors, B cells, CD4+ cells, IFN-γ, and nitric oxide on the level of parasitemia and parasite clearance during acute babesiosis. We found that B. microti reaches high parasitemia levels during the first week of infection in all three mice strains before resolving spontaneously. Our results indicate that resolution of babesiosis requires CD4 T cells and a novel mechanism of parasite killing within infected erythrocytes.

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Section: Discussioncontrasting

confidence: 73%

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Skariah

Arnaboldi

Dattwyler

et al. 2017

The Journal of Immunology

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“…Similar results suggesting the role of B cells in immune response regulation have been described in other murine models for autoimmune diseases, such as rheumatoid arthritis (RA) [9], autoimmune diabetes [10], and systemic lupus erythematosus (SLE) [11] as well as cancer [12] and other models of infectious diseases caused by bacteria, viruses, and parasites [13][14][15][16].…”

Section: B Cells As Immune Response Regulatorssupporting

confidence: 77%

Regulatory B Cells and Mechanisms

Rincón‐Arévalo

Sanchez-Parra

Castaño

et al. 2015

International Reviews of Immunology

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Regulatory B cells have gained prominence in their role as modulators of the immune response against tumors, infectious diseases, and autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis, among others. The concept of regulatory B cells has been strongly associated with interleukin (IL)-10 production; however, there is growing evidence that supports the existence of other regulatory mechanisms, such as the production of transforming growth factor β (TGF-β), induced cell death of effector T cells, and the induction of CD4(+)CD25(-)Foxp3(+) regulatory T cells. The regulatory function of B cells has been associated with the presence and activation of molecules such as CD40, CD19, CD1d, and BCR. Alterations in signaling by any of these pathways leads to a marked defect in regulatory B cells and to increased clinical symptoms and proinflammatory signs, both in murine models and in autoimmune diseases in humans. B cells mainly exert their regulatory effect through the inhibition of proliferation and production of proinflammatory mediators, such as TNF-α, IFN-γ, and IL-17 by CD4(+) T cells. A better understanding of how regulatory B cells function will offer new perspectives with regard to the treatment of various human diseases.

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“…The study by Ma, et al may be supported by this study. However, it should be noted that CD5, CD1d, or TIM-1 has not been established as surface markers in human regulatory B cells as opposed to mouse regulatory B cells 23,24…”

Section: Discussionmentioning

confidence: 99%

Regulatory B Cells Are Inversely Associated with Disease Activity in Rheumatoid Arthritis

et al. 2014

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PurposeThe function of regulatory B lymphocytes is known to be abnormal in inflammatory diseases. However, a recent study indicates that IL-10+ B cells seem to be expanded in rheumatoid arthritis (RA). Therefore, the state of IL-10+ B cells in the peripheral blood from RA patients and healthy controls were investigated.Materials and MethodsCD19+ cells in peripheral blood mononuclear cells were purified from blood samples of RA patients and age and gender-matched healthy controls, and stimulated with CD40 ligand and CpG for 48 hours. Then, intracellular IL-10 in CD19+ cells was analyzed using flow cytometry.ResultsThere was no significant difference in the proportion of IL-10+ B cells between 10 RA patients and 10 healthy controls (RA, 0.300±0.07 vs. healthy control 0.459±0.07, p=0.114). The proportion of induced IL-10+ B cells to total B cells in RA patients was significantly higher than those in controls (RA, 4.44±3.44% vs. healthy control 2.44±1.64%, p=0.033). However, the proportion of IL-10+ B cells to total B cells correlated negatively with disease activity in RA patients (r=-0.398, p=0.040). Erythrocyte sedimentation rate or C-reactive protein or medication was not associated with the proportion of IL-10+ B cells.ConclusionThe proportion of induced IL-10+ B cell increased in RA patients compared to healthy control, however, negatively correlated with disease activity in RA.

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Induction of IL-10-Producing CD1dhighCD5+ Regulatory B Cells following Babesia microti-Infection

Cited by 57 publications

References 22 publications

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Regulatory B Cells and Mechanisms

Regulatory B Cells Are Inversely Associated with Disease Activity in Rheumatoid Arthritis

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