Monoclonal auto-antibodies and sera of autoimmune patients react with Plasmodium falciparum and inhibit its in vitro growth

Brahimi, Karima; Martins, Yuri Chaves; Zaniní, Graziela Maria; Ferreira-da-Cruz, Maria de Fátima; Daniel-Ribeiro, Cláudio Tadeu

doi:10.1590/s0074-02762011000900006

Cited by 15 publications

(10 citation statements)

References 67 publications

(70 reference statements)

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“…In accordance, it has been recently found that autoantibodies and sera from patients suffering from diverse autoimmune conditions, but not from malaria, inhibit the in vitro growth of P. falciparum in human RBCs (Bhatnagar et al, 2011; Brahimi et al, 2011). Especially that type of autoimmunity is apparently required for protection against blood-stage malaria (Daniel-Ribeiro, 2000), that is presumably directed against autoantigens and parasite-induced neo-autoantigens on the surface of Plasmodium -infected RBCs (Wunderlich et al, 1988b,c; Fontaine et al, 2012).…”

Section: Liver Effectors Toward Blood-stage Malariamentioning

confidence: 67%

Liver-inherent immune system: its role in blood-stage malaria

2014

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The liver is well known as that organ which is obligately required for the intrahepatocyte development of the pre-erythrocytic stages of the malaria-causative agent Plasmodium. However, largely neglected is the fact that the liver is also a central player of the host defense against the morbidity- and mortality-causing blood stages of the malaria parasites. Indeed, the liver is equipped with a unique immune system that acts locally, however, with systemic impact. Its main “antipodal” functions are to recognize and to generate effective immunoreactivity against pathogens on the one hand, and to generate tolerance to avoid immunoreactivity with “self” and harmless substances as dietary compounds on the other hand. This review provides an introductory survey of the liver-inherent immune system: its pathogen recognition receptors including Toll-like receptors (TLRs) and its major cell constituents with their different facilities to fight and eliminate pathogens. Then, evidence is presented that the liver is also an essential organ to overcome blood-stage malaria. Finally, we discuss effector responses of the liver-inherent immune system directed against blood-stage malaria: activation of TLRs, acute phase response, phagocytic activity, cytokine-mediated pro- and anti-inflammatory responses, generation of “protective” autoimmunity by extrathymic T cells and B-1 cells, and T cell-mediated repair of liver injuries mainly produced by malaria-induced overreactions of the liver-inherent immune system.

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Section: Liver Effectors Toward Blood-stage Malariamentioning

confidence: 67%

Liver-inherent immune system: its role in blood-stage malaria

2014

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“…14-3-3 ε brain protein Degranulation of mast cells, basophils, eosinophils and/or monocytes/macrophages Protection against severe Plasmodium falciparum malaria Duarte et al, 2012 Beta tubulin III (TBB3) Cytoplasm microtubule disruption Cerebral malaria associated to P. falciparum Füchtbauer et al, 1985;Bansal et al, 2009 Dendritic tree of Purkinje cell In vitro inhibition of Purkinje cells development Cerebral malaria associated to P. falciparum Calvet et al, 1993;Gallien et al, 2011 Erythrocyte band 3 protein Rigidity increase and in vitro clearance of non-parasitized RBCs Anemia associated to Plasmodium vivax Mourão et al, 2016Mourão et al, , 2018 In vitro P. falciparum cythoadherence blockage and in vivo adherence of RBCs; parasite growth inhibition Protection against P. falciparum malaria Hogh et al, 1994 ;Brahimi et al, 2011 Lipids Kidney injury through immune complex deposition…”

Section: Clinical Outcome Referencesmentioning

confidence: 99%

“…This is the case of a study carried out in an area of intense transmission of malaria in Liberia, where it has been shown that immune responses to band 3 neoantigens are correlated with lower P. falciparum parasitemia and can block in vitro and in vivo RBCs' cytoadherence (Hogh et al, 1994). Moreover, an anti-plasmodial activity has been proposed to autoantibodies from patients with autoimmune diseases, which were able to inhibit parasite growth, suggesting a protective role for those molecules, although the authors have not ruled out the involvement of other serum components (Brahimi et al, 2011). Since the pathways involved in autoantibody-induced pathology differ among infections due to different parasites, it is possible that self-reactive antibodies exert diverse effects in infections by P. vivax and P. falciparum, an issue that should be target of future investigation.…”

Section: Clinical Outcome Referencesmentioning

confidence: 99%

Autoantibodies and Malaria: Where We Stand? Insights Into Pathogenesis and Protection

Mourão

Cardoso-Oliveira

Braga

2020

Front. Cell. Infect. Microbiol.

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Autoantibodies are frequently reported in patients with malaria, but whether they contribute to protection or to pathology is an issue of debate. A large body of evidence indicates that antibodies against host-self components are associated to malaria clinical outcomes such as cerebral malaria, renal dysfunction and anemia. Nonetheless, self-reactive immunoglobulins induced during an infection can also mediate protection. In light of these controversies, we summarize here the latest findings in our understanding of autoimmune responses in malaria, focusing on Plasmodium falciparum and Plasmodium vivax. We review the main targets of self-antibody responses in malaria as well as the current, but still limited, knowledge of their role in disease pathogenesis or protection.

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“…In fact, the serum samples of systemic lupus erythematosus (SLE) patients displayed the ability to recognize the Pf malarial antigens (40). Cardiolipin, histones, and DNA are among the auto-antigens usually targeted by the anti- Plasmodium antibodies (41).…”

Section: Activation Of B Cellsmentioning

confidence: 99%

To B or Not to B: Understanding B Cell Responses in the Development of Malaria Infection

2018

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Malaria is a widespread disease caused mainly by the Plasmodium falciparum (Pf) and Plasmodium vivax (Pv) protozoan parasites. Depending on the parasite responsible for the infection, high morbidity and mortality can be triggered. To escape the host immune responses, Plasmodium parasites disturb the functionality of B cell subsets among other cell types. However, some antibodies elicited during a malaria infection have the potential to block pathogen invasion and dissemination into the host. Thus, the question remains, why is protection not developed and maintained after the primary parasite exposure? In this review, we discuss different aspects of B cell responses against Plasmodium antigens during malaria infection. Since most studies have focused on the quantification of serum antibody titers, those B cell responses have not been fully characterized. However, to secrete antibodies, a complex cellular response is set up, including not only the activation and differentiation of B cells into antibody-secreting cells, but also the participation of other cell subsets in the germinal center reactions. Therefore, a better understanding of how B cell subsets are stimulated during malaria infection will provide essential insights toward the design of potent interventions.

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Monoclonal auto-antibodies and sera of autoimmune patients react with Plasmodium falciparum and inhibit its in vitro growth

Abstract: The relationship between autoimmunity and malaria is not well understood. To

Cited by 15 publications

References 67 publications

Liver-inherent immune system: its role in blood-stage malaria

Liver-inherent immune system: its role in blood-stage malaria

Autoantibodies and Malaria: Where We Stand? Insights Into Pathogenesis and Protection

To B or Not to B: Understanding B Cell Responses in the Development of Malaria Infection

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