Development of Plasmodium falciparum specific naïve, atypical, memory and plasma B cells during infancy and in adults in an endemic area

Lugaajju, Allan; Reddy, Sreenivasulu B.; Wahlgren, Mats; Kironde, Fred; Persson, Kristina

doi:10.1186/s12936-017-1697-z

Cited by 16 publications

(33 citation statements)

References 80 publications

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“…Consistent with the observation of febrile malaria children in Mali, malaria induces the activation of Th1 cytokines and Tfh-1 cells that contribute to the expansion of T-bet hi atypical MBCs, also causing reduced BCR signaling 25 . The study of development of MBCs in newborns and mother in malaria endemic area in Uganda showed an expansion of atypical MBCs and non-IgG + MBCs which increased with age 26 . In a low malaria transmission area in Brazil, found that single- and multiple- P .…”

Section: Discussionmentioning

confidence: 98%

Persistence of Long-lived Memory B Cells specific to Duffy Binding Protein in individuals exposed to Plasmodium vivax

Changrob

McHenry

Nyunt

et al. 2018

Sci Rep

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The major challenge in designing a protective Duffy binding protein region II (DBPII)-based vaccine against blood-stage vivax malaria is the high number of polymorphisms in critical residues targeted by binding-inhibitory antibodies. Here, longevity of antibody and memory B cell response (MBCs) to DBL-TH variants, DBL-TH2, -TH4, -TH5, -TH6 and -TH9 were analyzed in P. vivax-exposed individuals living in a low malaria transmission area of southern Thailand. Antibody to DBL-TH variants were significantly detected during P. vivax infection and it was persisted for up to 9 months post-infection. However, DBL-TH-specific MBC responses were stably maintained longer than antibody response, at least 3 years post-infection in the absence of re-infection. Phenotyping of B cell subsets showed the expansion of activated and atypical MBCs during acute and recovery phase of infection. While the persistence of DBL-TH-specific MBCs was found in individuals who had activated and atypical MBC expansion, anti-DBL-TH antibody responses was rapidly declined in plasma. The data suggested that these two MBCs were triggered by P. vivax infection, its expansion and stability may have impact on antibody responses. Our results provided evidence for ability of DBPII variant antigens in induction of long-lasting MBCs among individuals who were living in low malaria endemicity.

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Section: Discussionmentioning

confidence: 98%

Persistence of Long-lived Memory B Cells specific to Duffy Binding Protein in individuals exposed to Plasmodium vivax

Changrob

McHenry

Nyunt

et al. 2018

Sci Rep

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“…Additionally, the CMV+ group was defined by high titers of cord blood CMV IgM rather than the gold standard of neonatal CMV Ag or PCR detection in urine which was not feasible at the time of the study. We did not examine infectious disease Ag-specific MBC such as Pf-specific MBC which have been performed by Lugaajju et al and show Pf-specific MBC in various subsets (110). Also, inclusion of the two neonates with congenital CMV and exposed to HIV into the HIV exposed group could have influenced the results.…”

Section: Discussionmentioning

confidence: 99%

HIV, Cytomegalovirus, and Malaria Infections during Pregnancy Lead to Inflammation and Shifts in Memory B Cell Subsets in Kenyan Neonates

Yeo

Embury

Anderson

et al. 2019

The Journal of Immunology

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Infections during pregnancy can expose the fetus to microbial antigens leading to inflammation that affects B cell development. Prenatal fetal immune priming may have an important role in infant acquisition of pathogen specific immunity. We examined plasma pro-inflammatory biomarkers, the proportions of various B cell subsets, and fetal priming to tetanus vaccination in cord blood from human US and Kenyan neonates. US neonates had no identified prenatal infectious exposures whereas Kenyan neonates examined had congenital CMV or mothers with prenatal HIV or Plasmodium falciparum, or no identified infectious exposures. Kenyan neonates had higher levels of IP-10, TNFα, CRP, sCD14 and BAFF than US neonates. Among the Kenyan groups, neonates with prenatal infections/infectious exposures had higher levels of cord blood INFɣ, IL-7, sTNFR1 and sTNFR2 compared to neonates with no infectious exposures. Kenyan neonates had greater proportions of activated memory B cells (MBC) compared to US neonates. Among the Kenyan groups, HIV exposed neonates had greater proportions of atypical MBC compared to the other groups. Although HIV exposed neonates had altered MBC subset distributions, detection of tetanus-specific MBC from cord blood, indicative of fetal priming with tetanus vaccine given to pregnant women, was comparable in HIV exposed and non HIV exposed neonates. These results indicate that the presence of infections during pregnancy induces fetal immune activation with inflammation and increased activated MBC frequencies in neonates. The immunologic significance and long term health consequences of these differences warrants further investigation.

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“…Several observations suggest that P. falciparum infection per se drives the expansion of aMBCs including a positive correlation between aMBC expansion and intensity of P. falciparum transmission in studies primarily carried out in Africa including Mali (25, 26, 32), Uganda (28, 33, 34), Kenya (35, 36), the Gambia (37) and Ghana (38). Of interest, in HIV-malaria coinfected Rwandan adults the expansion of aMBC was greater as compared to that in individuals infected with malaria alone (39).…”

Section: Introductionmentioning

confidence: 99%

Atypical memory B cells in human chronic infectious diseases: An interim report

Portugal

Obeng-Adjei

Moir

et al. 2017

Cellular Immunology

161

177

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Immunological memory is a remarkable phenomenon in which survival of an initial infection by a pathogen leads to life-long protection from disease upon subsequent exposure to that same pathogen. For many infectious diseases, long-lived protective humoral immunity is induced after only a single infection in a process that depends on the generation of memory B cells (MBCs) and long-lived plasma cells. However, over the past decade it has become increasingly evident that many chronic human infectious diseases to which immunity is not readily established, including HIV-AIDS, malaria and TB, are associated with fundamental alterations in the composition and functionality of MBC compartments. A common feature of these diseases appears to be a large expansion of what have been termed exhausted B cells, tissue-like memory B cells or atypical memory B cells (aMBCs) that, for simplicity’s sake, we refer to here as aMBCs. It has been suggested that chronic immune activation and inflammation drive the expansion of aMBCs and that in some way aMBCs contribute to deficiencies in the acquisition of immunity in chronic infectious diseases. Although aMBCs are heterogeneous both within individuals and between diseases, they have several features in common including low expression of the cell surface markers that define classical MBCs in humans including CD21 and CD27 and high expression of genes not usually expressed by classical MBCs including T-bet, CD11c and a variety of inhibitory receptors, notably members of the FcRL family. Another distinguishing feature is their greatly diminished ability to be stimulated through their B cell receptors to proliferate, secrete cytokines or produce antibodies. In this review, we describe our current understanding of the phenotypic markers of aMBCs, their specificity in relation to the disease-causing pathogen, their functionality, the drivers of their expansion in chronic infections and their life span. We briefly summarize the features of aMBCs in healthy individuals and in autoimmune disease. We also comment on the possible relationship of human aMBCs and T-bet+, CD11c+ age/autoimmune-associated B cells, also a topic of this review volume.

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Development of Plasmodium falciparum specific naïve, atypical, memory and plasma B cells during infancy and in adults in an endemic area

Cited by 16 publications

References 80 publications

Persistence of Long-lived Memory B Cells specific to Duffy Binding Protein in individuals exposed to Plasmodium vivax

Persistence of Long-lived Memory B Cells specific to Duffy Binding Protein in individuals exposed to Plasmodium vivax

HIV, Cytomegalovirus, and Malaria Infections during Pregnancy Lead to Inflammation and Shifts in Memory B Cell Subsets in Kenyan Neonates

Atypical memory B cells in human chronic infectious diseases: An interim report

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