Malaria, caused by infection with protozoan parasites belonging to the genus Plasmodium, is a highly prevalent and lethal infectious disease, responsible for 445,000 deaths in 2016. Optimism that malaria was gradually being controlled and eliminated has been tampered by recent evidence that malaria control measures are beginning to stall and that Plasmodium parasites are developing resistance to front-line anti-malarial drugs. An important milestone has been the recent development of a malaria vaccine (Mosquirix) for use in humans, the very first against a parasitic infection. Unfortunately, this vaccine has modest and short-lived efficacy, with vaccinated individuals possibly being at increased risk of severe malarial disease when protection wanes. Thus, to define new ways to combat malaria, there remains an urgent requirement to identify the immune mechanisms that promote resistance to malarial disease and to understand why these so often fail.
Protection against malaria depends upon activation of innate immunity and on the generation of adaptive T and B cell responses. In particular, antibodies play a critical role in parasite control and prevention of severe malarial disease. Although the mechanisms and pathways through which the immune system recognizes and kills liver and blood-stage forms of Plasmodium parasites are beginning to be deciphered, emerging data also highlight that malaria parasites can directly and indirectly manipulate and subvert host immunity. This subsequently facilitates infection chronicity and susceptibility to re-infection. Conceptual and technical advances in our understanding of Plasmodium-host interactions will be essential to develop more effective vaccines for malaria and to devise new therapies for established malaria infection.
In this Research Topic, we aim to provide new insights into the processes that influence the immune response to Plasmodium infection and which shape vaccination strategies. We welcome the submission of Original Research, Review, Mini-Review and Clinical Trial articles covering, but not limited to, the following topics:
1. The development of vaccines and new immunotherapies for malaria.
2. Mechanisms of immune-mediated recognition and killing of Plasmodium parasites and infected cells during the liver or blood-stage of infection.
3. The role of monocytes, macrophages and dendritic cells in the immune response to Plasmodium infection.
4. Pathways that control T cell suppression and exhaustion during malaria.
5. The development of memory T cell populations following vaccination or natural Plasmodium infection and the mechanisms through which they provide protection against malaria.
6. The development of functional and atypical B cell populations during malaria and their role in protection against malaria.
7. The regulation of immune cell metabolism during Plasmodium infection.
We acknowledge the initiation and support of this Research Topic by the International Union of Immunological Societies (IUIS). We hereby state publicly that the IUIS has had no editorial input in articles included in this Research Topic, thus ensuring that all aspects of this Research Topic are evaluated objectively, unbiased by any specific policy or opinion of the IUIS.
Malaria, caused by infection with protozoan parasites belonging to the genus Plasmodium, is a highly prevalent and lethal infectious disease, responsible for 445,000 deaths in 2016. Optimism that malaria was gradually being controlled and eliminated has been tampered by recent evidence that malaria control measures are beginning to stall and that Plasmodium parasites are developing resistance to front-line anti-malarial drugs. An important milestone has been the recent development of a malaria vaccine (Mosquirix) for use in humans, the very first against a parasitic infection. Unfortunately, this vaccine has modest and short-lived efficacy, with vaccinated individuals possibly being at increased risk of severe malarial disease when protection wanes. Thus, to define new ways to combat malaria, there remains an urgent requirement to identify the immune mechanisms that promote resistance to malarial disease and to understand why these so often fail.
Protection against malaria depends upon activation of innate immunity and on the generation of adaptive T and B cell responses. In particular, antibodies play a critical role in parasite control and prevention of severe malarial disease. Although the mechanisms and pathways through which the immune system recognizes and kills liver and blood-stage forms of Plasmodium parasites are beginning to be deciphered, emerging data also highlight that malaria parasites can directly and indirectly manipulate and subvert host immunity. This subsequently facilitates infection chronicity and susceptibility to re-infection. Conceptual and technical advances in our understanding of Plasmodium-host interactions will be essential to develop more effective vaccines for malaria and to devise new therapies for established malaria infection.
In this Research Topic, we aim to provide new insights into the processes that influence the immune response to Plasmodium infection and which shape vaccination strategies. We welcome the submission of Original Research, Review, Mini-Review and Clinical Trial articles covering, but not limited to, the following topics:
1. The development of vaccines and new immunotherapies for malaria.
2. Mechanisms of immune-mediated recognition and killing of Plasmodium parasites and infected cells during the liver or blood-stage of infection.
3. The role of monocytes, macrophages and dendritic cells in the immune response to Plasmodium infection.
4. Pathways that control T cell suppression and exhaustion during malaria.
5. The development of memory T cell populations following vaccination or natural Plasmodium infection and the mechanisms through which they provide protection against malaria.
6. The development of functional and atypical B cell populations during malaria and their role in protection against malaria.
7. The regulation of immune cell metabolism during Plasmodium infection.
We acknowledge the initiation and support of this Research Topic by the International Union of Immunological Societies (IUIS). We hereby state publicly that the IUIS has had no editorial input in articles included in this Research Topic, thus ensuring that all aspects of this Research Topic are evaluated objectively, unbiased by any specific policy or opinion of the IUIS.
