Characterization of the Spleen B‐Cell Compartment at the Early and Late Blood‐Stage <i>Plasmodium chabaudi</i> Malaria

Castillo-Méndez, Sheyla Inés; Zago, Cláudia Augusta; Sardinha, Luiz Roberto; Rosário, Ana Paula Freitas do; Álvarez, José María; Lima, Maria Regina D'Império

doi:10.1111/j.1365-3083.2007.01972.x

Cited by 21 publications

(28 citation statements)

References 47 publications

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“…In contrast, there is no infection-induced apoptosis of FoB cells in the spleen. During Pc AS infection in mice, there are many class-switched plasma B cells found in both peripheral blood and spleen, comprising mostly IgG2a-secreting cells [42–45] that play an important role in parasite clearance. Most likely the conservation of the FoB cell pool during infection, being the major source for high-affinity malaria-specific class-switched plasma B cells, which in turn are essential for parasite clearance, allows the mouse to control the Pc AS infection.…”

Section: Discussionmentioning

confidence: 99%

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

Bockstal

Geurts

Magez

2011

Journal of Parasitology Research

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B cells and antibodies are essential for the protective immune response against a blood-stage Plasmodium infection. Although extensive research has focused on memory as well as plasma B-cell responses during infection, little is known about how malaria affects B-cell development and splenic maturation into marginal zone B (MZB) and follicular B (FoB) cells. In this study, we show that acute Plasmodium chabaudi AS infection in C57Bl/6 mice causes severe disruption of B lymphopoiesis in the bone marrow, affecting in particular pro-, pre-, and immature B cells as well as the expression of the bone marrow B-cell retention chemokine CXCL12. In addition, elevated apoptosis of transitional T2 and marginal zone (MZ) B cells was observed during and subsequent to the control of the first wave of parasitemia. In contrast, Folllicular (Fo) B cells levels were retained in the spleen throughout the infection, suggesting that these are essential for parasite clearance and proper infection control.

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Section: Discussionmentioning

confidence: 99%

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

Bockstal

Geurts

Magez

2011

Journal of Parasitology Research

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“…These B cells participate in a first line of defense against bacterial, viral, and parasitic infections (19,(37)(38)(39)(40)(41)(42)(43)(44)(45). MZ B cells encounter invading blood-borne pathogens early based on their anatomical localization in the marginal sinus of the spleen.…”

mentioning

confidence: 99%

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

Malkiel

Kuhlow

Mena

et al. 2009

The Journal of Immunology

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T cell-independent Abs are protective against Lyme disease and relapsing fever, illnesses caused by Borrelia spirochetes with distinct blood-borne phases of infection. To understand this protective response, we characterized splenic and peritoneal B cell compartments during infection using flow cytometry and immunohistochemistry. In the spleen, early after infection, Borrelia crocidurae, a relapsing fever species, induced a striking loss of marginal zone (MZ) B cells from the MZ, while Borrelia burgdorferi, the agent of Lyme disease, induced the expansion of this subset. At the same time, no significant changes were observed in follicular B cells in response to either species of Borrelia. In the peritoneal cavity, a further loss was demonstrated early in response to B. crocidurae in the B1b, B1c, and B2 cell subsets, but B1a cells were not significantly altered. The loss of B1c and B2 cells was sustained through subsequent peaks of spirochetemia, suggesting these subsets may be important in resolving relapsing episodes. In contrast, an early and significant increase in peritoneal B1a, B1b, and B1c cells, but not B2 cells, occurred in response to B. burgdorferi. Later in the course of infection, both species of Borrelia induced the selective expansion of peritoneal B1b cells, suggesting that B1b cells may participate in long-lasting immunity to Lyme and relapsing fever spirochetes. Our data demonstrate that different Borrelia can activate the same B cell subsets in distinct ways and they each elicit a complex interplay of MZ and multiple peritoneal B cell subsets in the early response to infection.

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“…(Supplemental Fig. 2; (36, 37)). These events lead to a decline in mature B cell numbers in the spleen (Supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice

Ghosh

Wikenheiser

Kennedy

et al. 2016

The Journal of Immunology

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Hematopoietic stem and progenitor cells (HSPCs) function to replenish the immune cell repertoire under steady-state conditions, and in response to inflammation due to infection or stress. While the bone marrow serves as the primary niche for hematopoiesis, extramedullary mobilization and differentiation of HSPCs occurs in the spleen during acute Plasmodium infection –n a critical step in the host immune response. Here, we identified an atypical HSPC population in the spleen of C57BL/6 mice, with a Lineage−Sca-1+c-kit− (LSK−) phenotype that proliferates in response to infection with non-lethal Plasmodium yoelii 17X. Infection-derived LSK− cells upon transfer into naïve congenic mice were found to differentiate predominantly into mature follicular B cells. However, when transferred into infection-matched hosts, infection-derived LSK− cells gave rise to B cells capable of entering into a germinal center reaction, and developed into memory B cells and antibody-secreting cells that were capable of producing parasite-specific antibodies. Differentiation of LSK− cells into B cells in vitro was enhanced in the presence of parasitized RBC lysate, suggesting that LSK− cells expand and differentiate in direct response to the parasite. However, the ability of LSK− cells to differentiate into B cells was not dependent on MyD88 as myd88−/− LSK− cell expansion and differentiation remained unaffected after Plasmodium infection. Collectively, these data identify a population of atypical lymphoid progenitors that differentiate into B-lymphocytes in the spleen, and are capable of contributing to the ongoing humoral immune response against Plasmodium infection.

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Characterization of the Spleen B‐Cell Compartment at the Early and Late Blood‐Stage Plasmodium chabaudi Malaria

Cited by 21 publications

References 47 publications

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

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

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

An Atypical Splenic B Cell Progenitor Population Supports Antibody Production during Plasmodium Infection in Mice

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