Protection against malaria in mice is induced by blood stage-arresting histamine-releasing factor (HRF)-deficient parasites
Although most vaccines against blood stage malaria in development today use subunit preparations, live attenuated parasites confer significantly broader and more lasting protection. In recent years, Plasmodium genetically attenuated parasites (GAPs) have been generated in rodent models that cause se...
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| Veröffentlicht in: | The Journal of experimental medicine 2016-07, Vol.213 (8), p.1419-1428 |
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| creator | Demarta-Gatsi, Claudia Smith, Leanna Thiberge, Sabine Peronet, Roger Commere, Pierre-Henri Matondo, Mariette Apetoh, Lionel Bruhns, Pierre Ménard, Robert Mécheri, Salaheddine |
| description | Although most vaccines against blood stage malaria in development today use subunit preparations, live attenuated parasites confer significantly broader and more lasting protection. In recent years, Plasmodium genetically attenuated parasites (GAPs) have been generated in rodent models that cause self-resolving blood stage infections and induce strong protection. All such GAPs generated so far bear mutations in housekeeping genes important for parasite development in red blood cells. In this study, using a Plasmodium berghei model compatible with tracking anti-blood stage immune responses over time, we report a novel blood stage GAP that lacks a secreted factor related to histamine-releasing factor (HRF). Lack of HRF causes an IL-6 increase, which boosts T and B cell responses to resolve infection and leave a cross-stage, cross-species, and lasting immunity. Mutant-induced protection involves a combination of antiparasite IgG2c antibodies and FcγR(+) CD11b(+) cell phagocytes, especially neutrophils, which are sufficient to confer protection. This immune-boosting GAP highlights an important role of opsonized parasite-mediated phagocytosis, which may be central to protection induced by all self-resolving blood stage GAP infections. |
| doi_str_mv | 10.1084/jem.20151976 |
| format | Article |
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In recent years, Plasmodium genetically attenuated parasites (GAPs) have been generated in rodent models that cause self-resolving blood stage infections and induce strong protection. All such GAPs generated so far bear mutations in housekeeping genes important for parasite development in red blood cells. In this study, using a Plasmodium berghei model compatible with tracking anti-blood stage immune responses over time, we report a novel blood stage GAP that lacks a secreted factor related to histamine-releasing factor (HRF). Lack of HRF causes an IL-6 increase, which boosts T and B cell responses to resolve infection and leave a cross-stage, cross-species, and lasting immunity. Mutant-induced protection involves a combination of antiparasite IgG2c antibodies and FcγR(+) CD11b(+) cell phagocytes, especially neutrophils, which are sufficient to confer protection. 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| subjects | Animals Antibodies, Protozoan - immunology B-Lymphocytes - immunology Biomarkers, Tumor - genetics Disease Models, Animal Female Immunoglobulin G - immunology Immunology Interleukin-6 - immunology Life Sciences Malaria - genetics Malaria - immunology Mice Neutrophils - immunology Phagocytosis - immunology Plasmodium berghei Plasmodium berghei - genetics Plasmodium berghei - immunology Protozoan Proteins - genetics Protozoan Proteins - immunology T-Lymphocytes - immunology |
| title | Protection against malaria in mice is induced by blood stage-arresting histamine-releasing factor (HRF)-deficient parasites |
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