B cell sub-types following acute malaria and associations with clinical immunity

Ssewanyana, Isaac; Wamala, Samuel; Nankya, Felistas; Jagannathan, Prasanna; Tappero, Jordan W.; Mayanja‐Kizza, Harriet; Muhindo, Mary; Arinaitwe, Emmanuel; Kamya, Moses R.; Dorsey, Grant; Feeney, Margaret E.; Riley, Eleanor M.; Drakeley, Chris; Greenhouse, Bryan; Sullivan, Richard

doi:10.1186/s12936-016-1190-0

Cited by 31 publications

(40 citation statements)

References 47 publications

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“…Malaria is characterized by many pathophysiological changes including alterations in the immune system involving myeloid‐cells, T‐cells and B‐cells. Regarding B‐cells, a number of observations clearly demonstrate that B‐cell homeostasis is affected by Plasmodium infection . This can be attributed to the complex biology of the parasites , their antigenic diversity , and their immune‐modulatory molecules .…”

Section: Discussionmentioning

confidence: 99%

Correlation of APRIL with production of inflammatory cytokines during acute malaria in the Brazilian Amazon

Pinna

Santos

Perce-da-Silva

et al. 2018

Immunity Inflam & Disease

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IntroductionA proliferation‐inducing ligand (APRIL) and B cell activation factor (BAFF) are known to play a significant role in the pathogenesis of several diseases, including BAFF in malaria. The aim of this study was to investigate whether APRIL and BAFF plasma concentrations could be part of inflammatory responses associated with P. vivax and P. falciparum malaria in patients from the Brazilian Amazon.MethodsBlood samples were obtained from P. vivax and P. falciparum malaria patients (n = 52) resident in Porto Velho before and 15 days after the beginning of treatment and from uninfected individuals (n = 12). We investigated APRIL and BAFF circulating levels and their association with parasitaemia, WBC counts, and cytokine/chemokine plasma levels. The expression levels of transmembrane activator and calcium‐modulating cyclophilin ligand interactor (TACI) on PBMC from a subset of 5 P. vivax‐infected patients were analyzed by flow cytometry.ResultsAPRIL plasma levels were transiently increased during acute P. vivax and P. falciparum infections whereas BAFF levels were only increased during acute P. falciparum malaria. Although P. vivax and P. falciparum malaria patients have similar cytokine profiles during infection, in P. vivax acute phase malaria, APRIL but not BAFF levels correlated positively with IL‐1, IL‐2, IL‐4, IL‐6, and IL‐13 levels. We did not find any association between P. vivax parasitaemia and APRIL levels, while an inverse correlation was found between P. falciparum parasitaemia and APRIL levels. The percentage of TACI positive CD4+ and CD8+ T cells were increased in the acute phase P. vivax malaria.ConclusionThese findings suggest that the APRIL and BAFF inductions reflect different host strategies for controlling infection with each malaria species.

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Section: Discussionmentioning

confidence: 99%

Correlation of APRIL with production of inflammatory cytokines during acute malaria in the Brazilian Amazon

Pinna

Santos

Perce-da-Silva

et al. 2018

Immunity Inflam & Disease

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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

165

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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“…However, functional impairment of AtMBCs present in P. falciparum ‐exposed children from Uganda, when delineated by upregulation of Fc‐receptor‐like 5 (FCRL5) and down‐modulation of B‐cell receptor (BCR) signalling demonstrated lower levels of antibody secretion . Expansion of AtMBC, in contrast to transitional B cells, was associated with clinical immunity following acute malaria . Combined, these studies highlight dynamic changes in B‐cell phenotype and function following acute and uncomplicated P. falciparum infections that may negatively impact antibody‐mediated immunity to malaria (Figure ).…”

Section: Antibody‐mediated Immunity and Cd4 T‐cell Helpmentioning

confidence: 97%

Immune effector mechanisms in malaria: An update focusing on human immunity

Moormann

Nixon

Forconi

2019

Parasite Immunology

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The past decade has witnessed dramatic decreases in malaria‐associated mortality and morbidity around the world. This progress has largely been due to intensified malaria control measures, implementation of rapid diagnostics and establishing a network to anticipate and mitigate antimalarial drug resistance. However, the ultimate tool for malaria prevention is the development and implementation of an effective vaccine. To date, malaria vaccine efforts have focused on determining which of the thousands of antigens expressed by Plasmodium falciparum are instrumental targets of protective immunity. The antigenic variation and antigenic polymorphisms arising in parasite genes under immune selection present a daunting challenge for target antigen selection and prioritization, and is a given caveat when interpreting immune recall responses or results from monovalent vaccine trials. Other immune evasion strategies executed by the parasite highlight the myriad of ways in which it can become a recurrent infection. This review provides an update on immune effector mechanisms in malaria and focuses on our improved ability to interrogate the complexity of human immune system, accelerated by recent methodological advances. Appreciating how the human immune landscape influences the effectiveness and longevity of antimalarial immunity will help explain which conditions are necessary for immune effector mechanisms to prevail.

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B cell sub-types following acute malaria and associations with clinical immunity

Cited by 31 publications

References 47 publications

Correlation of APRIL with production of inflammatory cytokines during acute malaria in the Brazilian Amazon

Correlation of APRIL with production of inflammatory cytokines during acute malaria in the Brazilian Amazon

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

Immune effector mechanisms in malaria: An update focusing on human immunity

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