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001-es BibID:	BIBFORM022981
Első szerző:	Ferreira, Ana
Cím:	Sickle Hemoglobin Confers Tolerance to Plasmodium Infection / Ferreira Ana, Marguti Ivo, Bechmann Ingo, Jeney Viktória, Chora Angelo, Palha Nuno R., Rebelo Sofia, Henri Annie, Beuzard Yves, Soares Miguel P.
Dátum:	2011
ISSN:	0092-8674
Megjegyzések:	Sickle human hemoglobin (Hb) confers a survival advantage to individuals living in endemic areas of malaria, the disease caused by Plasmodium infection. As demonstrated hereby, mice expressing sickle Hb do not succumb to experimental cerebral malaria (ECM). This protective effect is exerted irrespectively of parasite load, revealing that sickle Hb confers host tolerance to Plasmodium infection. Sickle Hb induces the expression of heme oxygenase-1 (HO-1) in hematopoietic cells, via a mechanism involving the transcription factor NF-E2-related factor 2 (Nrf2). Carbon monoxide (CO), a byproduct of heme catabolism by HO-1, prevents further accumulation of circulating free heme after Plasmodium infection, suppressing the pathogenesis of ECM. Moreover, sickle Hb inhibits activation and/or expansion of pathogenic CD8(+) T cells recognizing antigens expressed by Plasmodium, an immunoregulatory effect that does not involve Nrf2 and/or HO-1. Our findings provide insight into molecular mechanisms via which sickle Hb confers host tolerance to severe forms of malaria.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Cell. - 145 : 3 (2011), p. 398-409. -
További szerzők:	Marguti, Ivo Bechmann, Ingo Jeney Viktória (1971-) (vegyész, kémia tanár) Chora, Angelo Palha, Nuno R. Rebelo, Sofia Henri, Annie Beuzard, Yves Soares, Miguel P.
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001-es BibID:	BIBFORM078365
035-os BibID:	(WoS)000461679000073 (Scopus)85063288166 (PMID)30833408
Első szerző:	Ramos, Susana
Cím:	Renal control of disease tolerance to malaria / Susana Ramos, Ana Rita Carlos, Balamurugan Sundaram, Viktoria Jeney, Ana Ribeiro, Raffaella Gozzelino, Claudia Bank, Erida Gjini, Faouzi Braza, Rui Martins, Temitope Wilson Ademolue, Birte Blankenhaus, Zélia Gouveia, Pedro Faísca, Damian Trujillo, Sílvia Cardoso, Sofia Rebelo, Laura del Barrio, Abolfazl Zarjou, Subhashini Bolisetty, Anupam Agarwal, Miguel P. Soares
Dátum:	2019
ISSN:	0027-8424 1091-6490
Megjegyzések:	Malaria, the disease caused by Plasmodium spp. infection, remains a major global cause of morbidity and mortality. Host protection from malaria relies on immune-driven resistance mechanisms that kill Plasmodium However, these mechanisms are not sufficient per se to avoid the development of severe forms of disease. This is accomplished instead via the establishment of disease tolerance to malaria, a defense strategy that does not target Plasmodium directly. Here we demonstrate that the establishment of disease tolerance to malaria relies on a tissue damage-control mechanism that operates specifically in renal proximal tubule epithelial cells (RPTEC). This protective response relies on the induction of heme oxygenase-1 (HMOX1; HO-1) and ferritin H chain (FTH) via a mechanism that involves the transcription-factor nuclear-factor E2-related factor-2 (NRF2). As it accumulates in plasma and urine during the blood stage of Plasmodium infection, labile heme is detoxified in RPTEC by HO-1 and FTH, preventing the development of acute kidney injury, a clinical hallmark of severe malaria.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk disease tolerance heme infection kidney malaria
Megjelenés:	Proceedings of the National Academy of Sciences of the United States of America. - 116 : 12 (2019), p. 5681-5686. -
További szerzők:	Carlos, Ana Rita Sundaram, Balamurugan Jeney Viktória (1971-) (vegyész, kémia tanár) Ribeiro, Ana Gozzelino, Raffaella Bank, Claudia Gjini, Erida Braza, Faouzi Martins, Rui Ademolue, Temitope Wilson Blankenhaus, Birte Gouveia, Zélia Faísca, Pedro Trujillo, Damian Cardoso, Sílvia Rebelo, Sofia del Barrio, Laura Zarjou, Abolfazl (1979-) (kutató orvos) Bolisetty, Subhashini Agarwal, Anupam Soares, Miguel P.
Pályázati támogatás:	OTKA-116024 OTKA
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