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Review
. 2019 Apr 2:10:559.
doi: 10.3389/fimmu.2019.00559. eCollection 2019.

Development of B Cell Memory in Malaria

Ann Ly  1   2 , Diana S Hansen  1   2
Affiliations
Review

Development of B Cell Memory in Malaria

Ann Ly et al. Front Immunol. .

Abstract

A single exposure to many viral and bacterial pathogens typically induces life-long immunity, however, the development of the protective immunity to Plasmodium parasites is strikingly less efficient and achieves only partial protection, with adults residing in endemic areas often experiencing asymptomatic infections. Although naturally acquired immunity to malaria requires both cell-mediated and humoral immune responses, antibodies govern the control of malarial disease caused by the blood-stage form of the parasites. A large body of epidemiological evidence described that antibodies to Plasmodium antigens are inefficiently generated and rapidly lost without continued parasite exposure, suggesting that malaria is accompanied by defects in the development of immunological B cell memory. This topic has been of focus of recent studies of malaria infection in humans and mice. This review examines the main findings to date on the processes that modulate the acquisition of memory B cell responses to malaria, and highlights the importance of closing outstanding gaps of knowledge in the field for the rational design of next generation therapeutics against malaria.

Keywords: antibodies; immunity; inflammation; malaria; memory B cells.

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Figures

Figure 1
Figure 1
Pathways leading to the development of B cell memory. Upon encounter with antigen, activated B cells in secondary lymphoid tissue receive helper signals from cognate CD4+ T cells at the border of the B cell follicle and T cell zones. Some of the proliferating B cells differentiate into short-lived plasmablasts that initiate an extrafollicular antibody response, some develop into early memory B cells independently of GC formation, while others aggregate into the follicle to establish a GC. Within the GC, B cells undergo proliferation and somatic hypermutation in the dark zone, followed by affinity-based selection in the light zone with the help of T follicular helper cells and follicular dendritic cells. Long-lived plasma cells and memory B cells emerge from the GC reaction. Upon antigen rechallenge, memory B cells lacking expression of the surface molecules CD80 and PD-L2, mainly of the IgM isotype, can seed secondary GCs, whereas those expressing both molecules, comprising of IgM and IgG isotypes, predominantly generate plasmablasts. GC, germinal center; DC, dendritic cell; SHM, somatic hypermutation.
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