Acute Disruption of Bone Marrow B Lymphopoiesis and Apoptosis of Transitional and Marginal Zone B Cells in the Spleen following a Blood-Stage<i>Plasmodium chabaudi</i>Infection in Mice

Bockstal, Viki; Geurts, Nathalie; Magez, Stefan

doi:10.1155/2011/534697

Cited by 40 publications

(45 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The majority of these subsets also showed reduced proportions in the B-cell compartment 3 days after drug treatment. While these reduced proportions are likely due to redistribution of B-cells from the circulation for instance to secondary lymphoid organs such as the spleen, we cannot exclude that there might also be a loss in B-cells due for example to apoptosis (47, 48). An explanation for these late proliferative responses might therefore be either a) the release of elsewhere recruited activated cells back into the circulation or b) a physiological counter reaction to replenish the apoptosis-diminished B-cell pool.…”

Section: Discussionmentioning

confidence: 99%

BAFF and BAFF Receptor Levels Correlate with B Cell Subset Activation and Redistribution in Controlled Human Malaria Infection

Scholzen

Teirlinck

Bijker

et al. 2014

The Journal of Immunology

View full text Add to dashboard Cite

Characteristic features of Plasmodium falciparum malaria are polyclonal B-cell activation and an altered composition of the blood B-cell compartment, including expansion of CD21−CD27− atypical memory B-cells. B-cell activating factor (BAFF) is a key cytokine in B-cell homeostasis, but its potential contribution to the modulation of the blood B-cell pool during malaria remains elusive. In the controlled human malaria model (CHMI) in malaria-naïve Dutch volunteers, we therefore examined the dynamics of BAFF induction and B-cell subset activation and composition, to investigate whether these changes are linked to malaria-induced immune activation and in particular induction of BAFF. Alterations in B-cell composition after CHMI closely resembled those observed in endemic areas. We further found distinct kinetics of proliferation for individual B-cell subsets across all developmental stages. Proliferation peaked either immediately after blood-stage infection or at convalescence, and for most subsets was directly associated with the peak parasitemia. Concomitantly, plasma BAFF levels during CHMI were increased and correlated with membrane-expressed BAFF on monocytes and dendritic cells, as well as blood-stage parasitemia and parasite-induced IFNγ. Correlating with elevated plasma BAFF and IFNγ levels, IgD−CD38lowCD21−CD27− atypical B-cells showed the strongest proliferative response of all memory B-cell subsets. This provides unique evidence for a link between malaria-induced immune activation and temporary expansion of this B-cell subset. Finally, baseline BAFF-receptor levels prior to CHMI were predictive of subsequent changes in proportions of individual B-cell subsets. These findings suggest an important role of BAFF in facilitating B-cell subset proliferation and redistribution as a consequence of malaria-induced immune activation.

show abstract

Section: Discussionmentioning

confidence: 99%

BAFF and BAFF Receptor Levels Correlate with B Cell Subset Activation and Redistribution in Controlled Human Malaria Infection

Scholzen

Teirlinck

Bijker

et al. 2014

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Both Trypanosoma and Plasmodium infections have been associated with clonal deletion of B cells, with or without B cell polyclonal activation and proliferation [81–84]. Thus, another potential explanation for the lack of durable, sterilizing protective immunity following chronic or repeated parasitic infections relates to the loss of both antigen-specific and bystander B cells.…”

Section: B Cell Dysfunction During Parasitic Infectionsmentioning

confidence: 99%

Dysfunctional Adaptive Immunity During Parasitic Infections

Zander¹,

Butler²

2014

CIR

View full text Add to dashboard Cite

Parasite-driven dysfunctional adaptive immunity represents an emerging hypothesis to explain the chronic or persistent nature of parasitic infections, as well as the observation that repeated exposure to most parasitic organisms fails to engender sterilizing immunity. This review discusses recent examples from clinical studies and experimental models of parasitic infection that substantiate the role for immune dysfunction in the inefficient generation and maintenance of potent anti-parasitic immunity. Better understanding of the complex interplay between parasites, host adaptive immunity, and relevant negative regulatory circuits will inform efforts to enhance resistance to chronic parasitic infections through vaccination or immunotherapy.

show abstract

“…Disruption of the GC reaction has been shown to result in diminished production of classswitched, high-affinity Abs (59). In addition, P. chabaudi infection has been shown to affect B cell lymphopoiesis and the maturation of B cells into marginal zone or follicular B cells (60). These defects in B cell development could impact GC responses and the development of both B cell memory and long-lived Ab responses.…”

Section: Discussionmentioning

confidence: 99%

Acute Plasmodium chabaudi Infection Dampens Humoral Responses to a Secondary T-Dependent Antigen but Enhances Responses to a Secondary T-Independent Antigen

Wilmore

Maue

Lefebvre

et al. 2013

The Journal of Immunology

View full text Add to dashboard Cite

High rates of coinfection occur in malaria endemic regions, leading to more severe disease outcomes. Understanding how coinfecting pathogens influence the immune system is important in the development of treatment strategies that reduce morbidity and mortality. Using the Plasmodium chabaudi mouse model of malaria and immunization with model Ags that are either T-dependent (4-hydroxy-3-nitrophenyl [NP]-OVA) or T-independent (NP-Ficoll), we analyzed the effects of acute malaria on the development of humoral immunity to secondary Ags. Total Ig and IgG1 NP–specific Ab responses to NP-OVA were significantly decreased in the P. chabaudi–infected group compared with the uninfected group, whereas NP-specific IgG2c Ab was significantly increased in the P. chabaudi–infected group. In contrast, following injection with T-independent NP-Ficoll, the P. chabaudi–infected group had significantly increased NP-specific total Ig, IgM, and IgG2c Ab titers compared with controls. Treatment with anti–IFN-γ led to an abrogation of the NP-specific IgG2c Ab induced by P. chabaudi infection but did not affect other NP-specific Ab isotypes or titers. IFN-γ depletion also increased the percentage of plasma cells in both P. chabaudi–infected and uninfected groups but decreased the percentage of B cells with a germinal center (GC) phenotype. Using immunofluorescent microscopy, we were able to detect NP+ GCs in the spleens of noninfected mice, but there were no detectible NP+ GCs in mice infected with P. chabaudi. These data suggest that during P. chabaudi infection, there is a shift toward an extrafollicular Ab response that could be responsible for decreased Ab responses to secondary T-dependent Ags.

show abstract

Acute Disruption of Bone Marrow B Lymphopoiesis and Apoptosis of Transitional and Marginal Zone B Cells in the Spleen following a Blood-StagePlasmodium chabaudiInfection in Mice

Cited by 40 publications

References 50 publications

BAFF and BAFF Receptor Levels Correlate with B Cell Subset Activation and Redistribution in Controlled Human Malaria Infection

BAFF and BAFF Receptor Levels Correlate with B Cell Subset Activation and Redistribution in Controlled Human Malaria Infection

Dysfunctional Adaptive Immunity During Parasitic Infections

Acute Plasmodium chabaudi Infection Dampens Humoral Responses to a Secondary T-Dependent Antigen but Enhances Responses to a Secondary T-Independent Antigen

Contact Info

Product

Resources

About