Abstract
Malaria reflects not only a state of immune activation, but also a state of general immune defect or immunosuppression, of complex etiology that can last longer than the actual episode. Inhabitants of malaria-endemic regions with lifelong exposure to the parasite show an exhausted or immune regulatory profile compared to non- or minimally exposed subjects. Several studies and experiments to identify and characterize the cause of this malaria-related immunosuppression have shown that malaria suppresses humoral and cellular responses to both homologous (Plasmodium) and heterologous antigens (e.g., vaccines). However, neither the underlying mechanisms nor the relative involvement of different types of immune cells in immunosuppression during malaria is well understood. Moreover, the implication of the parasite during the different stages of the modulation of immunity has not been addressed in detail. There is growing evidence of a role of immune regulators and cellular components in malaria that may lead to immunosuppression that needs further research. In this review, we summarize the current evidence on how malaria parasites may directly and indirectly induce immunosuppression and investigate the potential role of specific cell types, effector molecules and other immunoregulatory factors.
Highlights
The limited effectiveness of the control measures applied since the beginning of the century has shown that the eradication of malaria is not easy to achieve
Almost as old as the concept of tolerance to malaria infections [31] is the concept of immunosuppression by malaria parasites, which was postulated after the observation of coincidental paratyphoid C fever during the malaria outbreaks in British Guiana in Epidemiological evidence of immunosuppression in relation to Plasmodium spp. infections were noted from different observations, starting with the perception that the incidence of rheumatoid arthritis and other autoimmune processes are less frequent in people exposed to malaria compared to people sharing a similar genetic background [33]
Plasmodium-specific atypical memory B cells (aMBCs) have been shown to proliferate in the body at similar frequencies as the classical memory B cells (MBCs), but have a shorter life span [62,108,128,129], which generates shorter specific responses against the parasite, maintained only under its presence [108,128]. This short effect is supported by the observation that in controlled human malaria infections (CHMI) in malaria-naïve individuals, aMBCs proliferate promptly throughout the course of the infection, suggesting that they do not originate from the germinal centers (GC) and do not follow memory generation [118]
Summary
The limited effectiveness of the control measures applied since the beginning of the century has shown that the eradication of malaria is not easy to achieve. Throughout childhood, repeated infective bites are needed to create a tolerance to malaria symptoms and partially to maintain antibodies and death, naturally acquired immunity is only effective andagainst tendscirto be shortculating. Which may result acquired in disease complications, and parasite multiplication be short-lived if exposure ceases This leads to a balance between controlling immune with the Downregulation of the inflammatory response upon the repeated encounters overactivation, which may otherwise result in disease complications, and parasite multiparasite ensues, and symptoms occur only if a higher threshold of parasitemia is reached plication [16,17,18]. Naturally acquired immunity must develop gradually acquire tolerance to clinical malaria quickly after an initial infection [21].from the prevention of symptoms to fullacquired parasite controlmust following over long. The information gathered here may help in optimizing immunization approaches in malaria endemic populations for better acquisition of protective immunity
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