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.
Highlights
Reviewed by: Julius Clemence Hafalla, London School of Hygiene and Tropical Medicine (LSHTM), United Kingdom Robin Stephens, The University of Texas Medical Branch at Galveston, United States
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
CONCLUDING REMARKS AND FUTURE PERSPECTIVES. Emerging evidence both in human field studies and murine infection models are beginning to address how the induction of humoral immune responses is compromised during acute malaria, and the consequences of these processes for the establishment of long-term immunological B cell memory
Summary
Immunological memory refers to the ability of the vertebrate immune system to remember previously encountered antigens or pathogens and evoke an enhanced immune response to control infection. The capacity of the host to generate T and B cell memory underlies the basis of protective immunity induced by vaccination or after exposure to specific pathogens. The generation of T celldependent humoral immune memory in secondary lymphoid organs (Figure 1) typically begins following B cell engagement with its cognate antigen, which triggers their migration to the B cell follicle border to receive T cell help [1]. The GC reaction leads to the generation of affinity-matured MBCs and long-lived plasma cells that contribute to host protection against re-infection. Plasma cells migrate to the bone marrow and provide a continuous source of circulating high-affinity antibody [7], while MBCs recirculate in the blood and secondary lymphoid tissue [8] to induce a rapid effector response upon antigen re-encounter [9, 10]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
