To B or Not to B: Understanding B Cell Responses in the Development of Malaria Infection

Abstract

Malaria is a widespread disease caused mainly by the Plasmodium falciparum (Pf) and Plasmodium vivax (Pv) protozoan parasites. Depending on the parasite responsible for the infection, high morbidity and mortality can be triggered. To escape the host immune responses, Plasmodium parasites disturb the functionality of B cell subsets among other cell types. However, some antibodies elicited during a malaria infection have the potential to block pathogen invasion and dissemination into the host. Thus, the question remains, why is protection not developed and maintained after the primary parasite exposure? In this review, we discuss different aspects of B cell responses against Plasmodium antigens during malaria infection. Since most studies have focused on the quantification of serum antibody titers, those B cell responses have not been fully characterized. However, to secrete antibodies, a complex cellular response is set up, including not only the activation and differentiation of B cells into antibody-secreting cells, but also the participation of other cell subsets in the germinal center reactions. Therefore, a better understanding of how B cell subsets are stimulated during malaria infection will provide essential insights toward the design of potent interventions.

Pathogenic Th1 responses in CHIKV‐induced inflammation and their modulation upon Plasmodium parasites co‐infection

“…This has been proposed as a mechanism to avoid the establishment of efficient and long‐lasting humoral responses . Notably, the development of naturally acquired immunity against Plasmodium is very slow and might take several years and is associated with a very low frequency of Plasmodium ‐specific memory B cells detected in populations from malaria endemic areas . Studies using murine and non‐human primate models have suggested impaired induction and maturation of germinal centers (GCs) thus leading to the production of low‐affinity, short‐lived antibody responses and the development of limited B cell memory.…”

“…This was supported by previous findings where apoptosis in lymph nodes and secondary lymphoid organs upon malaria infection was described. 133,134 In addition, it is also known that blood-stage malaria infections suppress dendritic cell (DC) responses by affecting DC maturation, [142][143][144] reducing surface expression of MHC-II 142,[145][146][147] and co-stimulatory molecule CD86, 146 inducing DC apoptosis 148,149 and impairing their ability to process and present parasite-derived antigens to T cells. 150,151 In line with this, reduced numbers of conventional DCs in the pLN of co-infected mice were also observed, suggesting that reduced expansion of CD4 + T cells might be due in part to the drop in DCs numbers associated with malaria.…”

“…This has been proposed as a mechanism to avoid the establishment of efficient and long-lasting humoral responses. 145 Notably, the development of naturally acquired immunity against Plasmodium is very slow and might take several years [146][147][148][149] and is associated with a very low frequency of Plasmodium-specific memory B cells detected in populations from malaria endemic areas. 150,151 Studies using murine and non-human primate models 107,132,146…”

Limited specificity of commercially available SARS-CoV-2 IgG ELISAs in serum samples of African origin

“…Although performance data for several of these assays have been rapidly communicated by different laboratories (4)(5)(6)(7)(8), to our knowledge no reports are available yet on the applicability of these tests on African serum panels. Here, assay specificity may be challenged by previous or current infections with other pathogens; in particular, hypergammaglobulinemia induced by Plasmodium infection may cause false positive results in serological tests (9,10).…”

Usando a imunologia de sistemas para entender os mecanismos moleculares de doenças e vacinas

“…A transcrição de um lncRNA (bloco laranja) pode afetar positivamente (1) ou negativamente (2 e 3) a expressão de um gene codificador de proteína (blocos azuis) através da indução de remodelamento da cromatina ou da inibição do recrutamento da RNA polimerase II e silenciamento epigenético, respectivamente. A hibridização de um lncRNA antisenso (bloco rosa) com um mRNA senso (blocos azuis) pode levar à degradação do mRNA (4) ou ao bloqueio do reconhecimento de um exon (bloco roxo) pelo spliceossomo causando uma alteração no padrão de splicing do mRNA (5). LncRNAs (bloco preto) também podem ser processados em RNAs pequenos como microRNAs, piRNAs, dentre outros (6).…”