Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells.

Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and e...
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Autor*in:	Jasmin Akter [verfasserIn] David S Khoury [verfasserIn] Rosemary Aogo [verfasserIn] Lianne I M Lansink [verfasserIn] Arya SheelaNair [verfasserIn] Bryce S Thomas [verfasserIn] Pawat Laohamonthonkul [verfasserIn] Clara P S Pernold [verfasserIn] Matthew W A Dixon [verfasserIn] Megan S F Soon [verfasserIn] Lily G Fogg [verfasserIn] Jessica A Engel [verfasserIn] Trish Elliott [verfasserIn] Ismail Sebina [verfasserIn] Kylie R James [verfasserIn] Deborah Cromer [verfasserIn] Miles P Davenport [verfasserIn] Ashraful Haque [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Übergeordnetes Werk:	In: PLoS Pathogens - Public Library of Science (PLoS), 2005, 15(2019), 2, p e1007599
Übergeordnetes Werk:	volume:15 ; year:2019 ; number:2, p e1007599

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1371/journal.ppat.1007599

Katalog-ID:	DOAJ049118072

Internformat


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520			\|a Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC.
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allfields	10.1371/journal.ppat.1007599 doi (DE-627)DOAJ049118072 (DE-599)DOAJ39969c1b306b4b6d93575b28a7501a6c DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Jasmin Akter verfasserin aut Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells. 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC. Immunologic diseases. Allergy Biology (General) David S Khoury verfasserin aut Rosemary Aogo verfasserin aut Lianne I M Lansink verfasserin aut Arya SheelaNair verfasserin aut Bryce S Thomas verfasserin aut Pawat Laohamonthonkul verfasserin aut Clara P S Pernold verfasserin aut Matthew W A Dixon verfasserin aut Megan S F Soon verfasserin aut Lily G Fogg verfasserin aut Jessica A Engel verfasserin aut Trish Elliott verfasserin aut Ismail Sebina verfasserin aut Kylie R James verfasserin aut Deborah Cromer verfasserin aut Miles P Davenport verfasserin aut Ashraful Haque verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 15(2019), 2, p e1007599 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:15 year:2019 number:2, p e1007599 https://doi.org/10.1371/journal.ppat.1007599 kostenfrei https://doaj.org/article/39969c1b306b4b6d93575b28a7501a6c kostenfrei http://europepmc.org/articles/PMC6411214?pdf=render kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2019 2, p e1007599
spelling	10.1371/journal.ppat.1007599 doi (DE-627)DOAJ049118072 (DE-599)DOAJ39969c1b306b4b6d93575b28a7501a6c DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Jasmin Akter verfasserin aut Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells. 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC. Immunologic diseases. Allergy Biology (General) David S Khoury verfasserin aut Rosemary Aogo verfasserin aut Lianne I M Lansink verfasserin aut Arya SheelaNair verfasserin aut Bryce S Thomas verfasserin aut Pawat Laohamonthonkul verfasserin aut Clara P S Pernold verfasserin aut Matthew W A Dixon verfasserin aut Megan S F Soon verfasserin aut Lily G Fogg verfasserin aut Jessica A Engel verfasserin aut Trish Elliott verfasserin aut Ismail Sebina verfasserin aut Kylie R James verfasserin aut Deborah Cromer verfasserin aut Miles P Davenport verfasserin aut Ashraful Haque verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 15(2019), 2, p e1007599 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:15 year:2019 number:2, p e1007599 https://doi.org/10.1371/journal.ppat.1007599 kostenfrei https://doaj.org/article/39969c1b306b4b6d93575b28a7501a6c kostenfrei http://europepmc.org/articles/PMC6411214?pdf=render kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2019 2, p e1007599
allfields_unstemmed	10.1371/journal.ppat.1007599 doi (DE-627)DOAJ049118072 (DE-599)DOAJ39969c1b306b4b6d93575b28a7501a6c DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Jasmin Akter verfasserin aut Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells. 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC. Immunologic diseases. Allergy Biology (General) David S Khoury verfasserin aut Rosemary Aogo verfasserin aut Lianne I M Lansink verfasserin aut Arya SheelaNair verfasserin aut Bryce S Thomas verfasserin aut Pawat Laohamonthonkul verfasserin aut Clara P S Pernold verfasserin aut Matthew W A Dixon verfasserin aut Megan S F Soon verfasserin aut Lily G Fogg verfasserin aut Jessica A Engel verfasserin aut Trish Elliott verfasserin aut Ismail Sebina verfasserin aut Kylie R James verfasserin aut Deborah Cromer verfasserin aut Miles P Davenport verfasserin aut Ashraful Haque verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 15(2019), 2, p e1007599 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:15 year:2019 number:2, p e1007599 https://doi.org/10.1371/journal.ppat.1007599 kostenfrei https://doaj.org/article/39969c1b306b4b6d93575b28a7501a6c kostenfrei http://europepmc.org/articles/PMC6411214?pdf=render kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2019 2, p e1007599
allfieldsGer	10.1371/journal.ppat.1007599 doi (DE-627)DOAJ049118072 (DE-599)DOAJ39969c1b306b4b6d93575b28a7501a6c DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Jasmin Akter verfasserin aut Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells. 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC. Immunologic diseases. Allergy Biology (General) David S Khoury verfasserin aut Rosemary Aogo verfasserin aut Lianne I M Lansink verfasserin aut Arya SheelaNair verfasserin aut Bryce S Thomas verfasserin aut Pawat Laohamonthonkul verfasserin aut Clara P S Pernold verfasserin aut Matthew W A Dixon verfasserin aut Megan S F Soon verfasserin aut Lily G Fogg verfasserin aut Jessica A Engel verfasserin aut Trish Elliott verfasserin aut Ismail Sebina verfasserin aut Kylie R James verfasserin aut Deborah Cromer verfasserin aut Miles P Davenport verfasserin aut Ashraful Haque verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 15(2019), 2, p e1007599 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:15 year:2019 number:2, p e1007599 https://doi.org/10.1371/journal.ppat.1007599 kostenfrei https://doaj.org/article/39969c1b306b4b6d93575b28a7501a6c kostenfrei http://europepmc.org/articles/PMC6411214?pdf=render kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2019 2, p e1007599
allfieldsSound	10.1371/journal.ppat.1007599 doi (DE-627)DOAJ049118072 (DE-599)DOAJ39969c1b306b4b6d93575b28a7501a6c DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Jasmin Akter verfasserin aut Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells. 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC. Immunologic diseases. Allergy Biology (General) David S Khoury verfasserin aut Rosemary Aogo verfasserin aut Lianne I M Lansink verfasserin aut Arya SheelaNair verfasserin aut Bryce S Thomas verfasserin aut Pawat Laohamonthonkul verfasserin aut Clara P S Pernold verfasserin aut Matthew W A Dixon verfasserin aut Megan S F Soon verfasserin aut Lily G Fogg verfasserin aut Jessica A Engel verfasserin aut Trish Elliott verfasserin aut Ismail Sebina verfasserin aut Kylie R James verfasserin aut Deborah Cromer verfasserin aut Miles P Davenport verfasserin aut Ashraful Haque verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 15(2019), 2, p e1007599 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:15 year:2019 number:2, p e1007599 https://doi.org/10.1371/journal.ppat.1007599 kostenfrei https://doaj.org/article/39969c1b306b4b6d93575b28a7501a6c kostenfrei http://europepmc.org/articles/PMC6411214?pdf=render kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2019 2, p e1007599
language	English
source	In PLoS Pathogens 15(2019), 2, p e1007599 volume:15 year:2019 number:2, p e1007599
sourceStr	In PLoS Pathogens 15(2019), 2, p e1007599 volume:15 year:2019 number:2, p e1007599
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Immunologic diseases. Allergy Biology (General)
isfreeaccess_bool	true
container_title	PLoS Pathogens
authorswithroles_txt_mv	Jasmin Akter @@aut@@ David S Khoury @@aut@@ Rosemary Aogo @@aut@@ Lianne I M Lansink @@aut@@ Arya SheelaNair @@aut@@ Bryce S Thomas @@aut@@ Pawat Laohamonthonkul @@aut@@ Clara P S Pernold @@aut@@ Matthew W A Dixon @@aut@@ Megan S F Soon @@aut@@ Lily G Fogg @@aut@@ Jessica A Engel @@aut@@ Trish Elliott @@aut@@ Ismail Sebina @@aut@@ Kylie R James @@aut@@ Deborah Cromer @@aut@@ Miles P Davenport @@aut@@ Ashraful Haque @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	501074422
id	DOAJ049118072
language_de	englisch
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callnumber-first	R - Medicine
author	Jasmin Akter
spellingShingle	Jasmin Akter misc RC581-607 misc QH301-705.5 misc Immunologic diseases. Allergy misc Biology (General) Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells.
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topic_title	RC581-607 QH301-705.5 Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells
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title	Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells.
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title_full	Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells
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author_browse	Jasmin Akter David S Khoury Rosemary Aogo Lianne I M Lansink Arya SheelaNair Bryce S Thomas Pawat Laohamonthonkul Clara P S Pernold Matthew W A Dixon Megan S F Soon Lily G Fogg Jessica A Engel Trish Elliott Ismail Sebina Kylie R James Deborah Cromer Miles P Davenport Ashraful Haque
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title_sort	plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells
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title_auth	Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells.
abstract	Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC.
abstractGer	Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC.
abstract_unstemmed	Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC.
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title_short	Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells.
url	https://doi.org/10.1371/journal.ppat.1007599 https://doaj.org/article/39969c1b306b4b6d93575b28a7501a6c http://europepmc.org/articles/PMC6411214?pdf=render https://doaj.org/toc/1553-7366 https://doaj.org/toc/1553-7374
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Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC.</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Immunologic diseases. 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Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells.

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